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ESP: PubMed Auto Bibliography 26 May 2026 at 01:57 Created:
Microbiome
It has long been known that every multicellular organism coexists with large prokaryotic ecosystems — microbiomes — that completely cover its surfaces, external and internal. Recent studies have shown that these associated microbiomes are not mere contamination, but instead have profound effects upon the function and fitness of the multicellular organism. We now know that all MCEs are actually functional composites, holobionts, composed of more prokaryotic cells than eukaryotic cells and expressing more prokaryotic genes than eukaryotic genes. A full understanding of the biology of "individual" eukaryotes will now depend on an understanding of their associated microbiomes.
Created with PubMed® Query: microbiome[tiab] NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2026-05-25
Circulating Short-Chain Fatty Acid (SCFA) profiles as a biomarker of gut-brain axis dysfunction: A meta-analysis for the SCFA signature in major depression.
Biomedical journal, 49(3):100968 pii:S2319-4170(26)00024-7 [Epub ahead of print].
BACKGROUND: Major Depressive Disorder (MDD) is increasingly viewed through the lens of the neuroinflammatory hypothesis and gut-brain axis dysfunction. Short-Chain Fatty Acids (SCFAs), the primary metabolites produced by the gut microbiota, are vital signaling molecules that maintain intestinal barrier integrity, modulate peripheral immunity, and influence microglial function. While individual studies suggest altered SCFAs levels in MDD, a definitive, quantitative synthesis establishing a robust biomarker signature is currently lacking. This meta-analysis aimed to precisely characterize the signature of SCFAs (acetic, propionic, butyric, and isobutyric acid) in MDD patients compared to healthy controls.
METHODS: We systematically searched major databases across PubMed, Embase, and Web of Science databases for studies quantifying SCFAs levels up to September 15, 2025. Studies examining SCFAs levels in depressed patients and depressive-like murine models, as well as studies investigating SCFAs interventions for depressive-like behavior, were selected for synthesis. Risk of bias was evaluated using the Newcastle-Ottawa Scale. The effect sizes were synthesized using a random-effects model and presented as standardized mean differences.
RESULTS: Eight human and 52 murine studies were included in the meta-analyses. Depressed patients showed significantly lower concentrations in blood (plasma and serum) of propionic (SMD = -0.60, p-value = 0.007), butyric (SMD = -0.50, p-value = 0.006), isobutyric (SMD = -0.72, p-value = 0.020), valeric (SMD = -0.43, p-value = 0.040) and isovaleric acids (SMD = -0.75, p-value = 0.002). Secondary analysis of MDD patients confirmed consistent reductions. High heterogeneity was observed. In murine models, SCFAs depletion was frequently observed, while supplementation improved depressive-like behaviors.
CONCLUSION: MDD is characterized by a significant, quantifiable deficit in the circulating SCFAs metabolome, which provides strong empirical validation for the gut-brain axis hypothesis in depression. We advocate for the investigation of SCFAs as novel, measurable peripheral biomarkers and targeted therapeutic agents (e.g., butyrate supplementation) for precision nutritional psychiatry.
Additional Links: PMID-41865792
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PubMed:
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@article {pmid41865792,
year = {2026},
author = {Do, QL and Malau, IA and Nguyen, HT and Liu, J and Chang, JP and Su, KP},
title = {Circulating Short-Chain Fatty Acid (SCFA) profiles as a biomarker of gut-brain axis dysfunction: A meta-analysis for the SCFA signature in major depression.},
journal = {Biomedical journal},
volume = {49},
number = {3},
pages = {100968},
doi = {10.1016/j.bj.2026.100968},
pmid = {41865792},
issn = {2320-2890},
abstract = {BACKGROUND: Major Depressive Disorder (MDD) is increasingly viewed through the lens of the neuroinflammatory hypothesis and gut-brain axis dysfunction. Short-Chain Fatty Acids (SCFAs), the primary metabolites produced by the gut microbiota, are vital signaling molecules that maintain intestinal barrier integrity, modulate peripheral immunity, and influence microglial function. While individual studies suggest altered SCFAs levels in MDD, a definitive, quantitative synthesis establishing a robust biomarker signature is currently lacking. This meta-analysis aimed to precisely characterize the signature of SCFAs (acetic, propionic, butyric, and isobutyric acid) in MDD patients compared to healthy controls.
METHODS: We systematically searched major databases across PubMed, Embase, and Web of Science databases for studies quantifying SCFAs levels up to September 15, 2025. Studies examining SCFAs levels in depressed patients and depressive-like murine models, as well as studies investigating SCFAs interventions for depressive-like behavior, were selected for synthesis. Risk of bias was evaluated using the Newcastle-Ottawa Scale. The effect sizes were synthesized using a random-effects model and presented as standardized mean differences.
RESULTS: Eight human and 52 murine studies were included in the meta-analyses. Depressed patients showed significantly lower concentrations in blood (plasma and serum) of propionic (SMD = -0.60, p-value = 0.007), butyric (SMD = -0.50, p-value = 0.006), isobutyric (SMD = -0.72, p-value = 0.020), valeric (SMD = -0.43, p-value = 0.040) and isovaleric acids (SMD = -0.75, p-value = 0.002). Secondary analysis of MDD patients confirmed consistent reductions. High heterogeneity was observed. In murine models, SCFAs depletion was frequently observed, while supplementation improved depressive-like behaviors.
CONCLUSION: MDD is characterized by a significant, quantifiable deficit in the circulating SCFAs metabolome, which provides strong empirical validation for the gut-brain axis hypothesis in depression. We advocate for the investigation of SCFAs as novel, measurable peripheral biomarkers and targeted therapeutic agents (e.g., butyrate supplementation) for precision nutritional psychiatry.},
}
RevDate: 2026-05-25
Skin-Brain Axis: Biological Foundations and Clinical Implications.
Journal of the Academy of Consultation-Liaison Psychiatry pii:S2667-2960(26)00049-2 [Epub ahead of print].
BACKGROUND: The skin-brain axis has emerged as a novel conceptual framework describing bidirectional neuroimmune, neuroendocrine, and microbial communication between the skin and the central nervous system. Shared inflammatory pathways, hypothalamic-pituitary-adrenal axis dysregulation, neurotransmitter signaling, neurotrophins, and microbiome-related mechanisms may contribute to the overlap between dermatologic and psychiatric disorders.
OBJECTIVE: To review the biological and clinical implications of the skin-brain axis in dermatologic and psychiatric disorders.
METHODS: This perspective review summarizes current evidence regarding the biological foundations and clinical implications of the skin-brain axis. The article integrates findings related to inflammatory skin disorders, psychiatric symptoms, immune signaling, microbial composition, and therapeutic approaches relevant to psychodermatology.
RESULTS: Evidence from psoriasis, atopic dermatitis, acne vulgaris, chronic urticaria, and prurigo nodularis demonstrates substantial overlap between inflammatory skin diseases and symptoms of depression, anxiety, stress, and suicidality. Emerging data further support the role of cutaneous immune signaling and microbial composition in modulating emotional and cognitive processes. The review also highlights therapeutic convergence between dermatology and psychiatry, including biologic therapies, psychopharmacology, cognitive behavioral therapy, and neuroimmune-targeted interventions.
CONCLUSIONS: Understanding the skin-brain axis may improve recognition of the bidirectional relationship between dermatologic and psychiatric disorders and support more comprehensive, integrated approaches to patients with complex inflammatory and neuropsychiatric conditions.
Additional Links: PMID-42031071
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PubMed:
Citation:
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@article {pmid42031071,
year = {2026},
author = {Ramirez-Posada, M and Guillen-Burgos, HF},
title = {Skin-Brain Axis: Biological Foundations and Clinical Implications.},
journal = {Journal of the Academy of Consultation-Liaison Psychiatry},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jaclp.2026.04.006},
pmid = {42031071},
issn = {2667-2960},
abstract = {BACKGROUND: The skin-brain axis has emerged as a novel conceptual framework describing bidirectional neuroimmune, neuroendocrine, and microbial communication between the skin and the central nervous system. Shared inflammatory pathways, hypothalamic-pituitary-adrenal axis dysregulation, neurotransmitter signaling, neurotrophins, and microbiome-related mechanisms may contribute to the overlap between dermatologic and psychiatric disorders.
OBJECTIVE: To review the biological and clinical implications of the skin-brain axis in dermatologic and psychiatric disorders.
METHODS: This perspective review summarizes current evidence regarding the biological foundations and clinical implications of the skin-brain axis. The article integrates findings related to inflammatory skin disorders, psychiatric symptoms, immune signaling, microbial composition, and therapeutic approaches relevant to psychodermatology.
RESULTS: Evidence from psoriasis, atopic dermatitis, acne vulgaris, chronic urticaria, and prurigo nodularis demonstrates substantial overlap between inflammatory skin diseases and symptoms of depression, anxiety, stress, and suicidality. Emerging data further support the role of cutaneous immune signaling and microbial composition in modulating emotional and cognitive processes. The review also highlights therapeutic convergence between dermatology and psychiatry, including biologic therapies, psychopharmacology, cognitive behavioral therapy, and neuroimmune-targeted interventions.
CONCLUSIONS: Understanding the skin-brain axis may improve recognition of the bidirectional relationship between dermatologic and psychiatric disorders and support more comprehensive, integrated approaches to patients with complex inflammatory and neuropsychiatric conditions.},
}
RevDate: 2026-05-22
CmpDate: 2026-05-22
Elucidating microbial succession and aroma-active metabolite formation in hybrid dry-fermented sausage analogues with texturized pea protein: Integrating flavoromics, metabolomics, and metagenomics.
Food research international (Ottawa, Ont.), 237:119324.
Hybrid dry-fermented sausage analogues with texturized pea proteins (TPPs) are emerging, yet flavor formation mechanisms remain unclear. We combined quantitative descriptive analysis with complementary HS-SPME-GC-MS/HS-GC-IMS volatilomics, UHPLC-MS/MS untargeted metabolomics, and marker-gene microbiome sequencing across sausages with different fermentation and ripening stages to map key aroma and their potential microbial and metabolic drivers. Sensory data showed rising fruity, cocoa-chocolate and nutty notes. In total, 47 volatiles were identified by GC-MS and 40 by GC-IMS. Screening of odorants based on relative odor activity value (rOAV) consistently highlighted seven odorants, with a shift from hexanal-dominated raw profiles to linalool-dominated processed profiles, indicating suppression of aldehyde-derived off-notes and enrichment of terpene/ester notes. Metabolomics detected 2467 metabolites, dominated by lipids and organic acids, and short-peptide enrichment suggested intensified proteolysis supplying aroma precursors. Bacterial succession exceeded fungal variation, with Latilactobacillus and Staphylococcus as core taxa. The integrated dataset provides practical markers and microbial/process cues to enhance flavor quality of sustainable hybrid fermented meats.
Additional Links: PMID-42169289
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PubMed:
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@article {pmid42169289,
year = {2026},
author = {Li, Y and Liu, X and Li, C and Xu, X and Tang, C and Zhou, G and Liu, Y and Blank, I},
title = {Elucidating microbial succession and aroma-active metabolite formation in hybrid dry-fermented sausage analogues with texturized pea protein: Integrating flavoromics, metabolomics, and metagenomics.},
journal = {Food research international (Ottawa, Ont.)},
volume = {237},
number = {},
pages = {119324},
doi = {10.1016/j.foodres.2026.119324},
pmid = {42169289},
issn = {1873-7145},
mesh = {*Metabolomics/methods ; *Meat Products/microbiology/analysis ; *Odorants/analysis ; Fermentation ; *Metagenomics/methods ; Volatile Organic Compounds/analysis ; *Pea Proteins/metabolism ; Animals ; Gas Chromatography-Mass Spectrometry ; Taste ; Food Microbiology ; Humans ; Microbiota ; Swine ; Tandem Mass Spectrometry ; },
abstract = {Hybrid dry-fermented sausage analogues with texturized pea proteins (TPPs) are emerging, yet flavor formation mechanisms remain unclear. We combined quantitative descriptive analysis with complementary HS-SPME-GC-MS/HS-GC-IMS volatilomics, UHPLC-MS/MS untargeted metabolomics, and marker-gene microbiome sequencing across sausages with different fermentation and ripening stages to map key aroma and their potential microbial and metabolic drivers. Sensory data showed rising fruity, cocoa-chocolate and nutty notes. In total, 47 volatiles were identified by GC-MS and 40 by GC-IMS. Screening of odorants based on relative odor activity value (rOAV) consistently highlighted seven odorants, with a shift from hexanal-dominated raw profiles to linalool-dominated processed profiles, indicating suppression of aldehyde-derived off-notes and enrichment of terpene/ester notes. Metabolomics detected 2467 metabolites, dominated by lipids and organic acids, and short-peptide enrichment suggested intensified proteolysis supplying aroma precursors. Bacterial succession exceeded fungal variation, with Latilactobacillus and Staphylococcus as core taxa. The integrated dataset provides practical markers and microbial/process cues to enhance flavor quality of sustainable hybrid fermented meats.},
}
MeSH Terms:
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*Metabolomics/methods
*Meat Products/microbiology/analysis
*Odorants/analysis
Fermentation
*Metagenomics/methods
Volatile Organic Compounds/analysis
*Pea Proteins/metabolism
Animals
Gas Chromatography-Mass Spectrometry
Taste
Food Microbiology
Humans
Microbiota
Swine
Tandem Mass Spectrometry
RevDate: 2026-05-22
CmpDate: 2026-05-22
Food-derived bioactive peptides in gut-muscle Axis regulation: Potential and challenges from microbiota homeostasis to muscle metabolism remodeling.
Food research international (Ottawa, Ont.), 237:119392.
The global population is aging at an accelerating pace, and sarcopenia has emerged as a central challenge to elderly health. Food-derived bioactive peptides, as natural functional compounds, can interact significantly with the gut microbiota, thereby indirectly influencing muscle metabolism and function. This review systematically summarizes the pathological mechanisms of sarcopenia and its associated complications. Moreover, it reveals the complex interactions between food-derived bioactive peptides and the gut microbiome, and innovatively summarizes the multi-level mechanisms by which these peptides regulate the gut-muscle axis. Furthermore, we discuss current research limitations, including the limited translational potential of animal models, insufficient precision of detection techniques, and lack of clinical validation. Future research directions are proposed, including leveraging multi-omics and artificial intelligence approaches for peptide-microbiota-metabolite functional prediction, employing organoid and organ-on-a-chip platforms for mechanistic validation, and advancing systematic translation through high-quality clinical trials. This review aims to provide a comprehensive theoretical framework and offer direction for the application of food-derived bioactive peptides based on gut-muscle axis interventions.
Additional Links: PMID-42169344
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@article {pmid42169344,
year = {2026},
author = {Song, H and Xue, S and Zhao, W and Yu, Z},
title = {Food-derived bioactive peptides in gut-muscle Axis regulation: Potential and challenges from microbiota homeostasis to muscle metabolism remodeling.},
journal = {Food research international (Ottawa, Ont.)},
volume = {237},
number = {},
pages = {119392},
doi = {10.1016/j.foodres.2026.119392},
pmid = {42169344},
issn = {1873-7145},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Peptides/metabolism ; Animals ; *Muscle, Skeletal/metabolism ; *Sarcopenia/metabolism ; Homeostasis ; Bioactive Peptides, Dietary ; },
abstract = {The global population is aging at an accelerating pace, and sarcopenia has emerged as a central challenge to elderly health. Food-derived bioactive peptides, as natural functional compounds, can interact significantly with the gut microbiota, thereby indirectly influencing muscle metabolism and function. This review systematically summarizes the pathological mechanisms of sarcopenia and its associated complications. Moreover, it reveals the complex interactions between food-derived bioactive peptides and the gut microbiome, and innovatively summarizes the multi-level mechanisms by which these peptides regulate the gut-muscle axis. Furthermore, we discuss current research limitations, including the limited translational potential of animal models, insufficient precision of detection techniques, and lack of clinical validation. Future research directions are proposed, including leveraging multi-omics and artificial intelligence approaches for peptide-microbiota-metabolite functional prediction, employing organoid and organ-on-a-chip platforms for mechanistic validation, and advancing systematic translation through high-quality clinical trials. This review aims to provide a comprehensive theoretical framework and offer direction for the application of food-derived bioactive peptides based on gut-muscle axis interventions.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Gastrointestinal Microbiome/physiology
*Peptides/metabolism
Animals
*Muscle, Skeletal/metabolism
*Sarcopenia/metabolism
Homeostasis
Bioactive Peptides, Dietary
RevDate: 2026-05-22
CmpDate: 2026-05-22
A systematic review of artificial intelligence and machine learning for gut microbiome-based CRC screening.
Journal of gastrointestinal oncology, 17(2):95.
BACKGROUND: Over the last decade, ample evidence has shown that gut microbiome dysbiosis is significantly associated with colorectal cancer (CRC). More recently, studies have shown that artificial intelligence (AI) and machine learning (ML) models paired with gut microbiome data can detect CRC. The objectives for this systematic review are: (I) to systematically evaluate the diagnostic performance of AI/ML models using gut microbiome data for CRC detection; (II) to compare AI/ML-based microbiome screening approaches; (III) to identify microbial genera consistently associated with CRC across included studies; (IV) to assess study quality and risk of bias using QUADAS-2 and use the GRADE approach to assess certainty.
METHODS: A systematic review was conducted across PubMed, MEDLINE, Scopus, Embase, and The Cochrane Library including studies from January 1, 2023 to November 1, 2025. Studies applying AI/ML models to human gut microbiome data for CRC screening and reporting diagnostic performance metrics and significant genera were included. Risk of bias was assessed with QUADAS-2 and used the GRADE approach to assess certainty. Primary outcomes included area under the receiver operating characteristic curve (AUC). Secondary outcomes include balanced accuracy, sensitivity, specificity, examine AI/ML approaches used, and identify significant microbial genera associated with CRC detected by AI/ML models. No meta-analysis was done due to the heterogeneity, which came from various microbiome methods, AI/ML/microbiome models used, and validation strategies applied. Thereby the data was synthesized narratively.
RESULTS: Twelve studies met inclusion criteria. AI/ML models demonstrated moderate diagnostic performance, with internal validation sets AUC values ranging from 0.61 to 0.98 and external validation sets AUC ranging from 0.70-0.87. Random forest and XGBoost models showed consistent performance, with multi-omics approaches achieving the highest AUC of 0.98. Porphyromonas (e.g., P. asaccharolytica), Peptostreptococcus (e.g., P. stomatis), Fusobacterium (particularly F. nucleatum subspecies: animalis, vincentii, polymorphum, sensu stricto), Parvimonas micra, Gemella morbillorum, Bacteroides (B. fragilis), and Streptococcus species were significantly enriched in CRC as predicted the selected AI/ML/microbiome models.
CONCLUSIONS: AI/ML-based gut microbiome models demonstrate moderate AUC for CRC detection and may enhance noninvasive screening strategies pending prospective validation. Limitations include heterogeneity in AI/ML/microbiome models, microbiome methodologies, and model validation, with predominantly retrospective case-control studies and limited external validation.
Additional Links: PMID-42169943
PubMed:
Citation:
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@article {pmid42169943,
year = {2026},
author = {Chittilla, M and Nagdev, P},
title = {A systematic review of artificial intelligence and machine learning for gut microbiome-based CRC screening.},
journal = {Journal of gastrointestinal oncology},
volume = {17},
number = {2},
pages = {95},
pmid = {42169943},
issn = {2078-6891},
abstract = {BACKGROUND: Over the last decade, ample evidence has shown that gut microbiome dysbiosis is significantly associated with colorectal cancer (CRC). More recently, studies have shown that artificial intelligence (AI) and machine learning (ML) models paired with gut microbiome data can detect CRC. The objectives for this systematic review are: (I) to systematically evaluate the diagnostic performance of AI/ML models using gut microbiome data for CRC detection; (II) to compare AI/ML-based microbiome screening approaches; (III) to identify microbial genera consistently associated with CRC across included studies; (IV) to assess study quality and risk of bias using QUADAS-2 and use the GRADE approach to assess certainty.
METHODS: A systematic review was conducted across PubMed, MEDLINE, Scopus, Embase, and The Cochrane Library including studies from January 1, 2023 to November 1, 2025. Studies applying AI/ML models to human gut microbiome data for CRC screening and reporting diagnostic performance metrics and significant genera were included. Risk of bias was assessed with QUADAS-2 and used the GRADE approach to assess certainty. Primary outcomes included area under the receiver operating characteristic curve (AUC). Secondary outcomes include balanced accuracy, sensitivity, specificity, examine AI/ML approaches used, and identify significant microbial genera associated with CRC detected by AI/ML models. No meta-analysis was done due to the heterogeneity, which came from various microbiome methods, AI/ML/microbiome models used, and validation strategies applied. Thereby the data was synthesized narratively.
RESULTS: Twelve studies met inclusion criteria. AI/ML models demonstrated moderate diagnostic performance, with internal validation sets AUC values ranging from 0.61 to 0.98 and external validation sets AUC ranging from 0.70-0.87. Random forest and XGBoost models showed consistent performance, with multi-omics approaches achieving the highest AUC of 0.98. Porphyromonas (e.g., P. asaccharolytica), Peptostreptococcus (e.g., P. stomatis), Fusobacterium (particularly F. nucleatum subspecies: animalis, vincentii, polymorphum, sensu stricto), Parvimonas micra, Gemella morbillorum, Bacteroides (B. fragilis), and Streptococcus species were significantly enriched in CRC as predicted the selected AI/ML/microbiome models.
CONCLUSIONS: AI/ML-based gut microbiome models demonstrate moderate AUC for CRC detection and may enhance noninvasive screening strategies pending prospective validation. Limitations include heterogeneity in AI/ML/microbiome models, microbiome methodologies, and model validation, with predominantly retrospective case-control studies and limited external validation.},
}
RevDate: 2026-05-22
CmpDate: 2026-05-22
PZLAST-MAG: full length protein sequence similarity search server of large-scale MAG proteins.
Bioinformatics advances, 6(1):vbag129.
MOTIVATION: Metagenome-assembled genomes (MAGs) provide access to novel protein sequences from uncultured microbes, offering invaluable resources for studying protein diversity, structure prediction, and evolutionary analysis. However, despite the explosive growth of MAG-derived protein data, tools enabling fast and accurate similarity searches against large-scale MAG protein datasets remain limited.
RESULTS: We present PZLAST-MAG, a web server for ultra-fast sequence similarity searches against 0.4 billion MAG-derived protein sequences (0.1 trillion amino acids) from over 210 000 MAGs indexed in Microbiome Datahub. Implemented on PEZY-SC3 MIMD many-core processors, PZLAST-MAG achieves high accuracy and speed, with performance comparable to widely used tools such as DIAMOND and MMseqs2 based on our benchmark analyses. In addition to tabular alignments, PZLAST-MAG provides interactive visualizations of phylogenetic and environmental distributions and co-occurrence patterns of homologous proteins across MAGs. This combination enables rapid homolog mining of functionally important genes across diverse microbial lineages while simultaneously revealing their taxonomic and ecological contexts. Two use case analyses indicate its utility for homolog mining of metabolic enzyme genes and plasmid-derived genes.
PZLAST-MAG is provided as a web-based service and is freely available at https://pzlast.nig.ac.jp/pzlast/mag without requiring registration.
Additional Links: PMID-42170025
PubMed:
Citation:
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@article {pmid42170025,
year = {2026},
author = {Higashi, K and Ishikawa, H and Kurokawa, K and Mori, H},
title = {PZLAST-MAG: full length protein sequence similarity search server of large-scale MAG proteins.},
journal = {Bioinformatics advances},
volume = {6},
number = {1},
pages = {vbag129},
pmid = {42170025},
issn = {2635-0041},
abstract = {MOTIVATION: Metagenome-assembled genomes (MAGs) provide access to novel protein sequences from uncultured microbes, offering invaluable resources for studying protein diversity, structure prediction, and evolutionary analysis. However, despite the explosive growth of MAG-derived protein data, tools enabling fast and accurate similarity searches against large-scale MAG protein datasets remain limited.
RESULTS: We present PZLAST-MAG, a web server for ultra-fast sequence similarity searches against 0.4 billion MAG-derived protein sequences (0.1 trillion amino acids) from over 210 000 MAGs indexed in Microbiome Datahub. Implemented on PEZY-SC3 MIMD many-core processors, PZLAST-MAG achieves high accuracy and speed, with performance comparable to widely used tools such as DIAMOND and MMseqs2 based on our benchmark analyses. In addition to tabular alignments, PZLAST-MAG provides interactive visualizations of phylogenetic and environmental distributions and co-occurrence patterns of homologous proteins across MAGs. This combination enables rapid homolog mining of functionally important genes across diverse microbial lineages while simultaneously revealing their taxonomic and ecological contexts. Two use case analyses indicate its utility for homolog mining of metabolic enzyme genes and plasmid-derived genes.
PZLAST-MAG is provided as a web-based service and is freely available at https://pzlast.nig.ac.jp/pzlast/mag without requiring registration.},
}
RevDate: 2026-05-22
CmpDate: 2026-05-22
Chemotherapy-induced peripheral neuropathy in breast cancer: a narrative review.
Translational breast cancer research : a journal focusing on translational research in breast cancer, 7:18.
BACKGROUND AND OBJECTIVE: Chemotherapy-induced peripheral neuropathy (CIPN) remains a major, unresolved complication of breast cancer therapy, often leading to treatment modifications and enduring functional impairment. This review addresses the complex pathogenesis of CIPN, as well as the clinical presentation and impact of CIPN on patient quality of life. The primary objective of this review is to highlight the pathophysiology and pathogenesis of CIPN, as well as detail current strategies and future targets to prevent and treat CIPN in breast cancer patients.
METHODS: We conducted a narrative review using the PubMed/Medline, Cochrane, and Embase databases from database inception to July 2025. We used keyword searches including 'breast cancer', 'chemotherapy-induced peripheral neuropathy/CIPN', 'taxane', 'taxane induced peripheral neuropathy/TIPN', 'platinum', 'alkaloids', 'antibody drug conjugates', 'CIPN prevention', 'CIPN treatment', 'biomarkers', 'microbiome', 'racial disparities', 'genetics', 'quality of life', 'inflammation'. Inclusion criteria included clinical and translational English-language studies addressing CIPN in breast cancer, CIPN biomarkers, and the microbiome in oncology research. Exclusion criteria included non-English language studies and clinical studies unrelated to breast cancer.
KEY CONTENT AND FINDINGS: In this paper, we synthesize the pathophysiology of CIPN and the growing body of research implicating systemic inflammation and gut microbiome composition in modulating CIPN pathogenesis, suggesting a biological basis for interindividual variability in susceptibility. We also summarize emerging evidence on the role of racial disparities in CIPN. Finally, we explore commonly studied biomarkers that have shown promise as potential predictive markers of CIPN onset as well as potential therapeutic strategies.
CONCLUSIONS: CIPN remains a common, dose-limiting toxicity in breast cancer care. Preventive strategies and symptomatic management with consistent clinical benefits are lacking. Duloxetine has strongest scientific evidence for pain reduction; other pharmacologic and non-pharmacologic approaches are promising but heterogeneous and should be framed as adjunctive. Biomarker driven trial designs that test anti-inflammatory strategies, as well as microbiome-targeted interventions, may accelerate treatment breakthroughs. Finally, attention to race as a factor in CIPN susceptibility can help to identify high-risk patients and reduce disparities in CIPN burden.
Additional Links: PMID-42170578
PubMed:
Citation:
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@article {pmid42170578,
year = {2026},
author = {Brodsky, M and Lalla, M and Oh, S and Anampa, JD},
title = {Chemotherapy-induced peripheral neuropathy in breast cancer: a narrative review.},
journal = {Translational breast cancer research : a journal focusing on translational research in breast cancer},
volume = {7},
number = {},
pages = {18},
pmid = {42170578},
issn = {2218-6778},
abstract = {BACKGROUND AND OBJECTIVE: Chemotherapy-induced peripheral neuropathy (CIPN) remains a major, unresolved complication of breast cancer therapy, often leading to treatment modifications and enduring functional impairment. This review addresses the complex pathogenesis of CIPN, as well as the clinical presentation and impact of CIPN on patient quality of life. The primary objective of this review is to highlight the pathophysiology and pathogenesis of CIPN, as well as detail current strategies and future targets to prevent and treat CIPN in breast cancer patients.
METHODS: We conducted a narrative review using the PubMed/Medline, Cochrane, and Embase databases from database inception to July 2025. We used keyword searches including 'breast cancer', 'chemotherapy-induced peripheral neuropathy/CIPN', 'taxane', 'taxane induced peripheral neuropathy/TIPN', 'platinum', 'alkaloids', 'antibody drug conjugates', 'CIPN prevention', 'CIPN treatment', 'biomarkers', 'microbiome', 'racial disparities', 'genetics', 'quality of life', 'inflammation'. Inclusion criteria included clinical and translational English-language studies addressing CIPN in breast cancer, CIPN biomarkers, and the microbiome in oncology research. Exclusion criteria included non-English language studies and clinical studies unrelated to breast cancer.
KEY CONTENT AND FINDINGS: In this paper, we synthesize the pathophysiology of CIPN and the growing body of research implicating systemic inflammation and gut microbiome composition in modulating CIPN pathogenesis, suggesting a biological basis for interindividual variability in susceptibility. We also summarize emerging evidence on the role of racial disparities in CIPN. Finally, we explore commonly studied biomarkers that have shown promise as potential predictive markers of CIPN onset as well as potential therapeutic strategies.
CONCLUSIONS: CIPN remains a common, dose-limiting toxicity in breast cancer care. Preventive strategies and symptomatic management with consistent clinical benefits are lacking. Duloxetine has strongest scientific evidence for pain reduction; other pharmacologic and non-pharmacologic approaches are promising but heterogeneous and should be framed as adjunctive. Biomarker driven trial designs that test anti-inflammatory strategies, as well as microbiome-targeted interventions, may accelerate treatment breakthroughs. Finally, attention to race as a factor in CIPN susceptibility can help to identify high-risk patients and reduce disparities in CIPN burden.},
}
RevDate: 2026-05-22
CmpDate: 2026-05-22
Distinct bile mycobiome signature identifies fungal peptide panel predictive for gallbladder carcinoma.
Molecular therapy. Oncology, 34(2):201220.
Carcinoma of the gallbladder (CAGB) carries a poor prognosis. While alterations in the bile microbiome and lipidome have been linked to CAGB development, the contribution of the fungal microbiome remains unexplored. We investigated fungal microbiome alterations and identified key fungal peptides capable of segregating CAGB patients. Bile samples from gallstone (GS) patients (n = 10), CAGB patients (n = 16), and healthy controls (n = 16) underwent fungal peptide-based diversity analysis and metabolomic profiling. Findings were cross-validated in plasma, correlated with clinical parameters and analyzed using machine learning. Six phyla and 24 fungal species were differentially regulated (p < 0.05). Alpha/beta diversity was higher in CAGB compared to GS and controls (p < 0.05). Ninety-three fungal peptides were upregulated and 63 downregulated in CAGB (p < 0.05, fold change [FC] > 1.5). CAGB patients showed significant enrichment of Aspergillus wentii (log2FC > 12.21), Nosema bombycis (FC > 11.25), Saccharomyces (FC > 10.89), Saccharomyces cerevisiae (FC > 10.68), and Schizosaccharomyces pombe (FC > 10.38). Fungal-metabolite correlations (r[2] > 0.5, p < 0.05) linked these taxa to lysine biosynthesis, taurine and hypotaurine metabolism, fatty acid metabolism in bile, and cysteine/methionine, ascorbate, and purine metabolism in plasma. Fungal peptide panel achieved 96% diagnostic efficiency for mortality prediction with>90% accuracy, sensitivity, and specificity. Bile fungal diversity correlates with CAGB development and identifies fungal peptide panel capable of segregation of CAGB patients.
Additional Links: PMID-42170678
PubMed:
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@article {pmid42170678,
year = {2026},
author = {Yadav, S and Sharma, N and Yadav, M and Sharma, N and Tripathi, G and Bhat, SH and Pandey, S and Mathew, B and Bindal, V and Saifi, R and Sharma, V and Falari, S and Pamecha, V and Maras, JS},
title = {Distinct bile mycobiome signature identifies fungal peptide panel predictive for gallbladder carcinoma.},
journal = {Molecular therapy. Oncology},
volume = {34},
number = {2},
pages = {201220},
pmid = {42170678},
issn = {2950-3299},
abstract = {Carcinoma of the gallbladder (CAGB) carries a poor prognosis. While alterations in the bile microbiome and lipidome have been linked to CAGB development, the contribution of the fungal microbiome remains unexplored. We investigated fungal microbiome alterations and identified key fungal peptides capable of segregating CAGB patients. Bile samples from gallstone (GS) patients (n = 10), CAGB patients (n = 16), and healthy controls (n = 16) underwent fungal peptide-based diversity analysis and metabolomic profiling. Findings were cross-validated in plasma, correlated with clinical parameters and analyzed using machine learning. Six phyla and 24 fungal species were differentially regulated (p < 0.05). Alpha/beta diversity was higher in CAGB compared to GS and controls (p < 0.05). Ninety-three fungal peptides were upregulated and 63 downregulated in CAGB (p < 0.05, fold change [FC] > 1.5). CAGB patients showed significant enrichment of Aspergillus wentii (log2FC > 12.21), Nosema bombycis (FC > 11.25), Saccharomyces (FC > 10.89), Saccharomyces cerevisiae (FC > 10.68), and Schizosaccharomyces pombe (FC > 10.38). Fungal-metabolite correlations (r[2] > 0.5, p < 0.05) linked these taxa to lysine biosynthesis, taurine and hypotaurine metabolism, fatty acid metabolism in bile, and cysteine/methionine, ascorbate, and purine metabolism in plasma. Fungal peptide panel achieved 96% diagnostic efficiency for mortality prediction with>90% accuracy, sensitivity, and specificity. Bile fungal diversity correlates with CAGB development and identifies fungal peptide panel capable of segregation of CAGB patients.},
}
RevDate: 2026-05-22
Ventilator-associated pneumonia: newer insights that can drive improved outcomes.
Current opinion in critical care pii:00075198-990000000-00361 [Epub ahead of print].
PURPOSE OF REVIEW: Ventilator-associated pneumonia (VAP) results in substantial morbidity and results in high crude mortality rates. Many recent studies address multiple aspects of VAP ranging from its evolving epidemiology and microbiology to novel means for prevention and treatment.
RECENT FINDINGS: The true incidence of VAP remains difficult to assess given definitional issues, which confound accurate diagnostic conclusions. The lack of a clear gold standard for identifying VAP makes comparisons across different studies difficult, as it remains unclear if like syndromes are actually being described. Nonetheless, VAP remains a clinical and costly challenge. Earlier discussion of achieving 'zero' VAP were clearly misplaced. Furthermore, the microbiology of VAP continues to evolve with the spread of antimicrobial resistance. New attention on the microbiome, though, may prove helpful and enhance our understanding of the pathogenesis of VAP. Simple interventions such a toothbrushing appear to successfully reduce rates of VAP and should be more broadly adopted. Rapid diagnostic tools, which are increasingly utilized to identify the causative pathogen in VAP, appear to have more limitations than previously thought. Several novel antibiotics are now available for treating multidrug-resistant organisms (MDROs) often encountered in VAP. With respect to antibiotic treatment more generally, it appears that shorter durations of therapy are well tolerated and effective, even in cases of VAP caused by MDROs.
SUMMARY: Although our knowledge and understanding of VAP continues to advance, many of the general questions of the last decade remain unresolved. We continue to lack a clear and simple means for defining VAP and have yet to identify the optimal approach for prevention. Likewise, despite the availability of newer antimicrobials, we continue to lack rapid diagnostics that can clearly be shown to improve patient-centered endpoints. The availability of newer antibiotics may allow us to more easily and safely treat MDROs, but they have not revolutionized outcomes or been shown to reduce mortality.
Additional Links: PMID-42170832
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PubMed:
Citation:
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@article {pmid42170832,
year = {2026},
author = {Shorr, AF and Zilberberg, MD},
title = {Ventilator-associated pneumonia: newer insights that can drive improved outcomes.},
journal = {Current opinion in critical care},
volume = {},
number = {},
pages = {},
doi = {10.1097/MCC.0000000000001390},
pmid = {42170832},
issn = {1531-7072},
abstract = {PURPOSE OF REVIEW: Ventilator-associated pneumonia (VAP) results in substantial morbidity and results in high crude mortality rates. Many recent studies address multiple aspects of VAP ranging from its evolving epidemiology and microbiology to novel means for prevention and treatment.
RECENT FINDINGS: The true incidence of VAP remains difficult to assess given definitional issues, which confound accurate diagnostic conclusions. The lack of a clear gold standard for identifying VAP makes comparisons across different studies difficult, as it remains unclear if like syndromes are actually being described. Nonetheless, VAP remains a clinical and costly challenge. Earlier discussion of achieving 'zero' VAP were clearly misplaced. Furthermore, the microbiology of VAP continues to evolve with the spread of antimicrobial resistance. New attention on the microbiome, though, may prove helpful and enhance our understanding of the pathogenesis of VAP. Simple interventions such a toothbrushing appear to successfully reduce rates of VAP and should be more broadly adopted. Rapid diagnostic tools, which are increasingly utilized to identify the causative pathogen in VAP, appear to have more limitations than previously thought. Several novel antibiotics are now available for treating multidrug-resistant organisms (MDROs) often encountered in VAP. With respect to antibiotic treatment more generally, it appears that shorter durations of therapy are well tolerated and effective, even in cases of VAP caused by MDROs.
SUMMARY: Although our knowledge and understanding of VAP continues to advance, many of the general questions of the last decade remain unresolved. We continue to lack a clear and simple means for defining VAP and have yet to identify the optimal approach for prevention. Likewise, despite the availability of newer antimicrobials, we continue to lack rapid diagnostics that can clearly be shown to improve patient-centered endpoints. The availability of newer antibiotics may allow us to more easily and safely treat MDROs, but they have not revolutionized outcomes or been shown to reduce mortality.},
}
RevDate: 2026-05-22
CmpDate: 2026-05-22
Effects of nifuratel-based therapy combined with vaginal lactobacillus probiotics on microecological restoration in pregnant women with abnormal vaginal flora: A retrospective cohort study.
Pakistan journal of pharmaceutical sciences, 39(7):1993-2002.
BACKGROUND: Imbalances in the vaginal flora during pregnancy elevate risks for adverse outcomes. While nifuratel targets pathogens, probiotics restore acidity, and robust cohort evidence supporting their combined safety and efficacy in restoring the microbiome remains limited.
OBJECTIVES: This retrospective cohort study assessed nifuratel-nystatin therapy plus Lactobacillus probiotics for restoring vaginal flora in pregnancy.
METHODS: Employing a retrospective cohort design, this study enrolled pregnant women diagnosed with vaginal microecological abnormalities between March 2023 and 2024. Participants were allocated via 1:1 propensity score matching (PSM) into two groups (n=58 each): a combination group receiving nifuratel-nystatin therapy combined with vaginal Lactobacillus probiotics and a monotherapy group receiving nifuratel-nystatin alone. All received a 7-day treatment. The primary endpoint was clinical effectiveness assessed one week post-treatment. Secondary outcomes included vaginal pH, Lactobacillus and bacterial diversity normalization rates, recurrence, adverse pregnancy outcomes and drug-related adverse events, monitored until delivery. Multivariate logistic regression identified independent predictors of treatment efficacy.
RESULTS: After PSM, baseline characteristics were balanced (P>0.05). The comparative analysis indicated a superior overall efficacy for the combination therapy (93.1%) over monotherapy (77.6%), with statistical significance (P<0.01) Both groups exhibited reduced vaginal pH and increased rates of normalized Lactobacillus and bacterial diversity, with greater improvements observed in the combination group (P<0.01). The recurrence rate was significantly lower in the combination group (8.6% vs. 22.4%; P<0.05), as was the total incidence of adverse pregnancy outcomes (6.9% vs. 20.7%; P<0.01). No significant difference in adverse drug reactions was found. Multivariate analysis identified combination therapy as an independent protective factor for clinical efficacy (aOR=4.25, 95% CI: 1.42-12.71, P<0.05).
CONCLUSIONS: In pregnant women with vaginal dysbiosis, combining nifuratel-nystatin with Lactobacillus probiotics safely enhances clinical efficacy, normalizes pH and flora and reduces adverse pregnancy outcomes.
Additional Links: PMID-42170966
Publisher:
PubMed:
Citation:
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@article {pmid42170966,
year = {2026},
author = {Luo, Y and Xu, H and Ye, X},
title = {Effects of nifuratel-based therapy combined with vaginal lactobacillus probiotics on microecological restoration in pregnant women with abnormal vaginal flora: A retrospective cohort study.},
journal = {Pakistan journal of pharmaceutical sciences},
volume = {39},
number = {7},
pages = {1993-2002},
doi = {10.36721/PJPS.2026.39.7.REG.189.1},
pmid = {42170966},
issn = {1011-601X},
mesh = {Female ; Humans ; Pregnancy ; *Probiotics/administration & dosage/therapeutic use/adverse effects ; Retrospective Studies ; Adult ; *Lactobacillus ; *Vagina/microbiology/drug effects ; Treatment Outcome ; *Microbiota/drug effects ; Young Adult ; Hydrogen-Ion Concentration ; },
abstract = {BACKGROUND: Imbalances in the vaginal flora during pregnancy elevate risks for adverse outcomes. While nifuratel targets pathogens, probiotics restore acidity, and robust cohort evidence supporting their combined safety and efficacy in restoring the microbiome remains limited.
OBJECTIVES: This retrospective cohort study assessed nifuratel-nystatin therapy plus Lactobacillus probiotics for restoring vaginal flora in pregnancy.
METHODS: Employing a retrospective cohort design, this study enrolled pregnant women diagnosed with vaginal microecological abnormalities between March 2023 and 2024. Participants were allocated via 1:1 propensity score matching (PSM) into two groups (n=58 each): a combination group receiving nifuratel-nystatin therapy combined with vaginal Lactobacillus probiotics and a monotherapy group receiving nifuratel-nystatin alone. All received a 7-day treatment. The primary endpoint was clinical effectiveness assessed one week post-treatment. Secondary outcomes included vaginal pH, Lactobacillus and bacterial diversity normalization rates, recurrence, adverse pregnancy outcomes and drug-related adverse events, monitored until delivery. Multivariate logistic regression identified independent predictors of treatment efficacy.
RESULTS: After PSM, baseline characteristics were balanced (P>0.05). The comparative analysis indicated a superior overall efficacy for the combination therapy (93.1%) over monotherapy (77.6%), with statistical significance (P<0.01) Both groups exhibited reduced vaginal pH and increased rates of normalized Lactobacillus and bacterial diversity, with greater improvements observed in the combination group (P<0.01). The recurrence rate was significantly lower in the combination group (8.6% vs. 22.4%; P<0.05), as was the total incidence of adverse pregnancy outcomes (6.9% vs. 20.7%; P<0.01). No significant difference in adverse drug reactions was found. Multivariate analysis identified combination therapy as an independent protective factor for clinical efficacy (aOR=4.25, 95% CI: 1.42-12.71, P<0.05).
CONCLUSIONS: In pregnant women with vaginal dysbiosis, combining nifuratel-nystatin with Lactobacillus probiotics safely enhances clinical efficacy, normalizes pH and flora and reduces adverse pregnancy outcomes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Female
Humans
Pregnancy
*Probiotics/administration & dosage/therapeutic use/adverse effects
Retrospective Studies
Adult
*Lactobacillus
*Vagina/microbiology/drug effects
Treatment Outcome
*Microbiota/drug effects
Young Adult
Hydrogen-Ion Concentration
RevDate: 2026-05-22
Circadian disruption elicits sex-specific gut microbiota, endocannabinoidome, and lipid mediator responses.
The FEBS journal [Epub ahead of print].
Circadian disruption is a pervasive environmental stressor associated with increased risk of metabolic and inflammatory disease, yet sex-specific physiological responses remain poorly defined. Here, we investigated how constant light (LL) exposure, used as a circadian stressor, is associated with changes in the fecal microbiome and short-chain fatty acids (SCFAs), tissue-specific bioactive lipid mediator and systemic cytokine levels in female and male mice. Mice were kept under standard light/dark (LD; 12 : 12) or LL (24 : 0) conditions for 10 days before feces collection and for 5 more days before tissue collection. Females exhibited broader microbiota restructuring along with decreases in oxylipins within the jejunum. In the brain pronounced increases of N-acylethanolamine levels in the cerebellum and hypothalamus were observed when male and female mice were analyzed together, though these changes were largely driven by increased levels in the hypothalamus of females. Changes in muscle lipids were associated with the predominant muscle fiber type, with the soleus showing increases in a broad variety of lipid classes in both females and males. Adipose tissues also showed divergent responses to LL, with subcutaneous white adipose tissue having significantly decreased oxylipin levels specifically in males. Within plasma, females generally showed a more inflammatory profile than males. Together, these findings suggest that sex strongly shapes microbial, lipidomic, and immune pathways changes under circadian stress, highlighting divergent physiological strategies in response to light-cycle perturbation, which may contribute to sex-specific vulnerability at the level of metabolic and inflammatory dysregulation.
Additional Links: PMID-42171003
Publisher:
PubMed:
Citation:
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@article {pmid42171003,
year = {2026},
author = {Pashaki, PA and Niepokny, TD and Khalilzadehsabet, T and Dumais, E and Flamand, N and Di Marzo, V and Mintz, EM and Silvestri, C},
title = {Circadian disruption elicits sex-specific gut microbiota, endocannabinoidome, and lipid mediator responses.},
journal = {The FEBS journal},
volume = {},
number = {},
pages = {},
doi = {10.1111/febs.70592},
pmid = {42171003},
issn = {1742-4658},
support = {R15GM134528/GF/NIH HHS/United States ; //Canadian Tri-Agency/ ; },
abstract = {Circadian disruption is a pervasive environmental stressor associated with increased risk of metabolic and inflammatory disease, yet sex-specific physiological responses remain poorly defined. Here, we investigated how constant light (LL) exposure, used as a circadian stressor, is associated with changes in the fecal microbiome and short-chain fatty acids (SCFAs), tissue-specific bioactive lipid mediator and systemic cytokine levels in female and male mice. Mice were kept under standard light/dark (LD; 12 : 12) or LL (24 : 0) conditions for 10 days before feces collection and for 5 more days before tissue collection. Females exhibited broader microbiota restructuring along with decreases in oxylipins within the jejunum. In the brain pronounced increases of N-acylethanolamine levels in the cerebellum and hypothalamus were observed when male and female mice were analyzed together, though these changes were largely driven by increased levels in the hypothalamus of females. Changes in muscle lipids were associated with the predominant muscle fiber type, with the soleus showing increases in a broad variety of lipid classes in both females and males. Adipose tissues also showed divergent responses to LL, with subcutaneous white adipose tissue having significantly decreased oxylipin levels specifically in males. Within plasma, females generally showed a more inflammatory profile than males. Together, these findings suggest that sex strongly shapes microbial, lipidomic, and immune pathways changes under circadian stress, highlighting divergent physiological strategies in response to light-cycle perturbation, which may contribute to sex-specific vulnerability at the level of metabolic and inflammatory dysregulation.},
}
RevDate: 2026-05-22
Metagenomic polymorphic toxin effector and immunity profiling predicts microbiome development and disease-related dysbiosis.
mSystems [Epub ahead of print].
Bacteria use antagonistic interbacterial weapons, such as polymorphic toxin secretion systems (TSS), to compete for niches in the human gut microbiome. We hypothesized that TSS influence gut microbiome development and disease-related dysbiosis. We developed a bioinformatic marker gene approach (PolyProf) to quantify TSS including ~200 effector and immunity genes and applied it to ~15,000 publicly available human metagenomes. PolyProf alpha and beta diversity readily distinguished 12 different human disease states and enabled the construction of highly accurate linear regression classifier machine learning models. Elastic net machine learning models integrating bacterial taxonomy with PolyProf had strong predictive value for 12 disease states, outperforming models utilizing taxonomy alone. During microbiome development in the first year of life, PolyProf alpha diversity increases, and beta diversity becomes increasingly like the maternal microbiome, influenced by vertical transfer, delivery mode, and breastfeeding. PolyProf is related to strain sharing among adults through social interactions. In summary, TSS genes strongly correlate with microbiome development and interpersonal strain sharing, suggesting roles for interbacterial antagonism. Since PolyProf distinguishes diverse adult disease statuses, these dynamics may contribute to non-genetic inheritance.IMPORTANCEPrevious research has demonstrated that bacteria compete within the gut microbiome using toxin secretion systems (TSS). How TSS contribute to human microbiome development and the microbiome alterations observed in human diseases is not known. This study develops a new bioinformatic tool for profiling TSS-related genes in metagenomic data. Application of this approach to large-scale human fecal metagenomic data demonstrates the dynamic association of TSS during microbiome development, including the exchange of strains among social contacts. TSS gene abundance patterns are highly predictive of 12 disease states. This study advances the field by enabling TSS profiling in metagenomes and by identifying disease and microbiome development biomarkers that provide hypotheses for future mechanistic studies and may be useful for disease diagnosis.
Additional Links: PMID-42171373
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PubMed:
Citation:
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@article {pmid42171373,
year = {2026},
author = {Schroer, HW and Beghini, F and Raygoza Garay, JA and Christakis, NA and Bosch, DE},
title = {Metagenomic polymorphic toxin effector and immunity profiling predicts microbiome development and disease-related dysbiosis.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0030526},
doi = {10.1128/msystems.00305-26},
pmid = {42171373},
issn = {2379-5077},
abstract = {Bacteria use antagonistic interbacterial weapons, such as polymorphic toxin secretion systems (TSS), to compete for niches in the human gut microbiome. We hypothesized that TSS influence gut microbiome development and disease-related dysbiosis. We developed a bioinformatic marker gene approach (PolyProf) to quantify TSS including ~200 effector and immunity genes and applied it to ~15,000 publicly available human metagenomes. PolyProf alpha and beta diversity readily distinguished 12 different human disease states and enabled the construction of highly accurate linear regression classifier machine learning models. Elastic net machine learning models integrating bacterial taxonomy with PolyProf had strong predictive value for 12 disease states, outperforming models utilizing taxonomy alone. During microbiome development in the first year of life, PolyProf alpha diversity increases, and beta diversity becomes increasingly like the maternal microbiome, influenced by vertical transfer, delivery mode, and breastfeeding. PolyProf is related to strain sharing among adults through social interactions. In summary, TSS genes strongly correlate with microbiome development and interpersonal strain sharing, suggesting roles for interbacterial antagonism. Since PolyProf distinguishes diverse adult disease statuses, these dynamics may contribute to non-genetic inheritance.IMPORTANCEPrevious research has demonstrated that bacteria compete within the gut microbiome using toxin secretion systems (TSS). How TSS contribute to human microbiome development and the microbiome alterations observed in human diseases is not known. This study develops a new bioinformatic tool for profiling TSS-related genes in metagenomic data. Application of this approach to large-scale human fecal metagenomic data demonstrates the dynamic association of TSS during microbiome development, including the exchange of strains among social contacts. TSS gene abundance patterns are highly predictive of 12 disease states. This study advances the field by enabling TSS profiling in metagenomes and by identifying disease and microbiome development biomarkers that provide hypotheses for future mechanistic studies and may be useful for disease diagnosis.},
}
RevDate: 2026-05-22
CmpDate: 2026-05-22
Skin Microbiome Variation Among Hosts and Batrachochytrium dendrobatidis Infection in Hyla meridionalis and Pelophylax perezi.
Molecular ecology, 35(10):e70393.
Chytridiomycosis, caused by the fungus Batrachochytrium dendrobatidis (Bd), is a key driver of global amphibian declines. The amphibian skin microbiome, which may include Bd-inhibitory bacteria, plays a crucial role in defence against infection, influencing host susceptibility and disease outcome. In this study, we investigated the skin microbiota and Bd infection in two frog species, Hyla meridionalis (Hm) and Pelophylax perezi (Pp), from northeastern Spain using full-length 16S rRNA gene sequencing. We found that microbiota composition differed significantly between frog species, with Pp harbouring greater bacterial richness and a community composition more similar to the aquatic environment than Hm. Asymptomatic Bd infection did not significantly alter microbiota diversity or community composition in either species. Nonetheless, differential abundance analyses revealed distinct bacterial taxa associated with host species and, to a lesser extent, with Bd infection. The composition of putative Bd-inhibitory bacteria also differed between frog species but was not influenced by Bd, suggesting that the microbiome's protective role may not be straightforward. Lower pathogen loads in Pp suggest a potential link between microbial richness and disease resistance. Our findings indicate that amphibian skin microbiota do not necessarily shift in response to Bd infection in asymptomatic hosts but may play a role in species-specific mechanisms of tolerance and resistance. Additionally, we detected potentially pathogenic bacteria of public and animal health concern on amphibian skin, highlighting amphibians as potential reservoirs and sentinels of ecosystem and public health. Overall, our findings indicate that amphibian skin microbiomes are shaped primarily by host species identity rather than asymptomatic Bd infection, emphasizing the importance of baseline microbiome variation in understanding host-pathogen dynamics and informing probiotic bioaugmentation strategies.
Additional Links: PMID-42171627
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PubMed:
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@article {pmid42171627,
year = {2026},
author = {Ribas, MP and Tort, C and Jasso, MV and Migura-Garcia, L and Cabezón, O},
title = {Skin Microbiome Variation Among Hosts and Batrachochytrium dendrobatidis Infection in Hyla meridionalis and Pelophylax perezi.},
journal = {Molecular ecology},
volume = {35},
number = {10},
pages = {e70393},
doi = {10.1111/mec.70393},
pmid = {42171627},
issn = {1365-294X},
support = {//Fundació Barcelona Zoo/ ; FI_B 00171//Departament de Recerca i Universitats, Generalitat de Catalunya, Spain/ ; //CERCA Program/ ; },
mesh = {Animals ; *Microbiota/genetics ; *Skin/microbiology ; *Batrachochytrium/pathogenicity ; RNA, Ribosomal, 16S/genetics ; *Ranidae/microbiology ; *Anura/microbiology ; Bacteria/genetics/classification ; *Mycoses/microbiology/veterinary ; Spain ; Chytridiomycota ; Skin Microbiome ; Animal Diseases ; },
abstract = {Chytridiomycosis, caused by the fungus Batrachochytrium dendrobatidis (Bd), is a key driver of global amphibian declines. The amphibian skin microbiome, which may include Bd-inhibitory bacteria, plays a crucial role in defence against infection, influencing host susceptibility and disease outcome. In this study, we investigated the skin microbiota and Bd infection in two frog species, Hyla meridionalis (Hm) and Pelophylax perezi (Pp), from northeastern Spain using full-length 16S rRNA gene sequencing. We found that microbiota composition differed significantly between frog species, with Pp harbouring greater bacterial richness and a community composition more similar to the aquatic environment than Hm. Asymptomatic Bd infection did not significantly alter microbiota diversity or community composition in either species. Nonetheless, differential abundance analyses revealed distinct bacterial taxa associated with host species and, to a lesser extent, with Bd infection. The composition of putative Bd-inhibitory bacteria also differed between frog species but was not influenced by Bd, suggesting that the microbiome's protective role may not be straightforward. Lower pathogen loads in Pp suggest a potential link between microbial richness and disease resistance. Our findings indicate that amphibian skin microbiota do not necessarily shift in response to Bd infection in asymptomatic hosts but may play a role in species-specific mechanisms of tolerance and resistance. Additionally, we detected potentially pathogenic bacteria of public and animal health concern on amphibian skin, highlighting amphibians as potential reservoirs and sentinels of ecosystem and public health. Overall, our findings indicate that amphibian skin microbiomes are shaped primarily by host species identity rather than asymptomatic Bd infection, emphasizing the importance of baseline microbiome variation in understanding host-pathogen dynamics and informing probiotic bioaugmentation strategies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Microbiota/genetics
*Skin/microbiology
*Batrachochytrium/pathogenicity
RNA, Ribosomal, 16S/genetics
*Ranidae/microbiology
*Anura/microbiology
Bacteria/genetics/classification
*Mycoses/microbiology/veterinary
Spain
Chytridiomycota
Skin Microbiome
Animal Diseases
RevDate: 2026-05-22
Taxonomic filtering accompanies functional expansion during long-term soil restoration.
The ISME journal pii:8690623 [Epub ahead of print].
The restoration of species-rich calcareous grasslands is a critical conservation objective, yet the recovery of the invisible below-ground microbiome remains poorly quantified compared to above-ground vegetation. Using a unique 143-year land-use chronosequence on Salisbury Plain, UK, we investigated the trajectory of ecosystem reassembly across arable, regenerating (23 and 67 years), and ancient grasslands. By integrating vegetation surveys with soil physiochemistry, microbial profiling, and shotgun metagenomics, we identified a decoupling between floral and edaphic recovery. While the diversity of vegetation recovered relatively rapidly, approaching ancient grassland levels within 23-67 years, soil properties exhibited persistent legacy effects and slow convergence. Bacterial richness decreased with restoration age; this taxonomic contraction was conversely matched by an expansion in inferred metagenomic functional potential. This was reflected in increased functional gene richness and shifts in the relative abundance of specific SEED-annotated functions toward metabolic pathways associated with complex carbon cycling and stress tolerance. These shifts were congruent with the emergence of specific, unnamed genera belonging to Pseudomonadota and Actinomycetota, and the Bacillota species Pristimantibacillus. The soil ecosystem remained distinct from the 143-year stage even after 67 years of recovery, characterised by persistent legacy phosphorus and a slow accumulation of soil organic matter. These findings suggest that passive regeneration alone may be insufficient for full soil functional recovery, and that strategies targeting microbial assembly and long-term carbon dynamics warrant further evaluation.
Additional Links: PMID-42171661
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PubMed:
Citation:
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@article {pmid42171661,
year = {2026},
author = {Goodall, T and Busi, SB and Jones, B and Thorpe, A and Griffiths, RI and Redhead, J and Hulmes, L and Hulmes, S and Ridding, L and Peyton, J and Pereira, G and Gweon, HS and Read, DS and Pywell, R},
title = {Taxonomic filtering accompanies functional expansion during long-term soil restoration.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag131},
pmid = {42171661},
issn = {1751-7370},
abstract = {The restoration of species-rich calcareous grasslands is a critical conservation objective, yet the recovery of the invisible below-ground microbiome remains poorly quantified compared to above-ground vegetation. Using a unique 143-year land-use chronosequence on Salisbury Plain, UK, we investigated the trajectory of ecosystem reassembly across arable, regenerating (23 and 67 years), and ancient grasslands. By integrating vegetation surveys with soil physiochemistry, microbial profiling, and shotgun metagenomics, we identified a decoupling between floral and edaphic recovery. While the diversity of vegetation recovered relatively rapidly, approaching ancient grassland levels within 23-67 years, soil properties exhibited persistent legacy effects and slow convergence. Bacterial richness decreased with restoration age; this taxonomic contraction was conversely matched by an expansion in inferred metagenomic functional potential. This was reflected in increased functional gene richness and shifts in the relative abundance of specific SEED-annotated functions toward metabolic pathways associated with complex carbon cycling and stress tolerance. These shifts were congruent with the emergence of specific, unnamed genera belonging to Pseudomonadota and Actinomycetota, and the Bacillota species Pristimantibacillus. The soil ecosystem remained distinct from the 143-year stage even after 67 years of recovery, characterised by persistent legacy phosphorus and a slow accumulation of soil organic matter. These findings suggest that passive regeneration alone may be insufficient for full soil functional recovery, and that strategies targeting microbial assembly and long-term carbon dynamics warrant further evaluation.},
}
RevDate: 2026-05-22
Analytic attributes of the 16S rRNA gene sequencing methodology for human gut microbiota characterization.
Applied microbiology and biotechnology pii:10.1007/s00253-026-13844-8 [Epub ahead of print].
Gut microbiota is crucial for human health. While 16S rRNA gene sequencing is most used for characterizing this community, the validation and standardization of the technique are often overlooked. This study analyzes critical factors influencing the repeatability and intermediate precision of 16S rRNA gene sequencing methodology for human gut microbiota characterization, examining the impact of key analytical factors. Our investigation evaluated the effects of the DNA extraction protocol, sample homogenization, thawing, library preparation, and sequencing on measurements of precision. This established a standardized operating procedure (SOP) whose variability was assessed within a single laboratory (intermediate precision) by analyzing DNA extraction kit lot variations and the laboratory analyst handling the samples. We discovered that the DNA extraction protocol and sample thawing were the most significant drivers of variability in gut microbiota profiles. At the same time, the intermediate precision of the method was high. We determined the method's limit of quantification, revealing an impressive sensitivity down to just 11 to 18 rarefied read counts (with coefficients of variation of 30% and 20%, respectively). Beyond technical considerations, we also quantified the variation in gut microbiota profiles among individuals and over time. Our findings confirm substantial inter-individual differences while demonstrating that changes within individuals over a week are relatively small. This research illuminates some critical factors influencing the precision and consistency of 16S rRNA gene sequencing for gut microbiota analysis. By incorporating these insights into standardized protocols, we can significantly improve best practices in DNA sequencing methodologies, strengthening the reliability and comparability of human microbiome studies. KEY POINTS: • DNA extraction and sample thawing critically affect the method's precision. • We established an SOP with high repeatability, intermediate precision, and a specific limit of quantification. • Gut microbiota profiles substantially vary among individuals but remain stable over a week.
Additional Links: PMID-42171783
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PubMed:
Citation:
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@article {pmid42171783,
year = {2026},
author = {Rivera, DA and Lara-Guzmán, OJ and Villota-Salazar, NA and Sierra, JA and Muñoz-Durango, K and Escobar, JS},
title = {Analytic attributes of the 16S rRNA gene sequencing methodology for human gut microbiota characterization.},
journal = {Applied microbiology and biotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00253-026-13844-8},
pmid = {42171783},
issn = {1432-0614},
abstract = {Gut microbiota is crucial for human health. While 16S rRNA gene sequencing is most used for characterizing this community, the validation and standardization of the technique are often overlooked. This study analyzes critical factors influencing the repeatability and intermediate precision of 16S rRNA gene sequencing methodology for human gut microbiota characterization, examining the impact of key analytical factors. Our investigation evaluated the effects of the DNA extraction protocol, sample homogenization, thawing, library preparation, and sequencing on measurements of precision. This established a standardized operating procedure (SOP) whose variability was assessed within a single laboratory (intermediate precision) by analyzing DNA extraction kit lot variations and the laboratory analyst handling the samples. We discovered that the DNA extraction protocol and sample thawing were the most significant drivers of variability in gut microbiota profiles. At the same time, the intermediate precision of the method was high. We determined the method's limit of quantification, revealing an impressive sensitivity down to just 11 to 18 rarefied read counts (with coefficients of variation of 30% and 20%, respectively). Beyond technical considerations, we also quantified the variation in gut microbiota profiles among individuals and over time. Our findings confirm substantial inter-individual differences while demonstrating that changes within individuals over a week are relatively small. This research illuminates some critical factors influencing the precision and consistency of 16S rRNA gene sequencing for gut microbiota analysis. By incorporating these insights into standardized protocols, we can significantly improve best practices in DNA sequencing methodologies, strengthening the reliability and comparability of human microbiome studies. KEY POINTS: • DNA extraction and sample thawing critically affect the method's precision. • We established an SOP with high repeatability, intermediate precision, and a specific limit of quantification. • Gut microbiota profiles substantially vary among individuals but remain stable over a week.},
}
RevDate: 2026-05-22
CmpDate: 2026-05-22
Microbiome in Gastrointestinal Tumors: Implications in Oncogenesis and Therapeutic Response : Microbiome in Gastrointestinal Tumors.
Current oncology reports, 28(1):.
PURPOSE OF REVIEW: To provide an updated overview of the role of the human microbiome in the initiation, progression, and therapeutic response of gastrointestinal tumors, emphasizing molecular, immunological, and metabolic mechanisms, as well as its potential as a target for novel therapeutic strategies.
RECENT FINDINGS: Emerging evidence demonstrates that microbiome dysbiosis contributes to carcinogenesis across gastrointestinal malignancies, including colorectal, gastric, hepatic, and pancreatic cancers. Microbial-derived metabolites, such as short-chain fatty acids and secondary bile acids, modulate key signaling pathways involved in cell proliferation, apoptosis, and genomic stability. In addition, the microbiome influences the tumor microenvironment and immune responses, shaping variability in treatment outcomes. Both preclinical and clinical studies have shown that microbiome composition affects the efficacy and toxicity of chemotherapy and immunotherapy. Notably, specific microbial signatures are being explored as non-invasive biomarkers for early detection and prognostic stratification, while microbiome modulation strategies, such as diet, probiotics, antibiotics, and fecal microbiota transplantation, have demonstrated potential to enhance therapeutic response. The bidirectional interaction between the microbiome and the host plays a central role in gastrointestinal tumorigenesis and treatment response. Although this field holds significant promise for precision oncology, its clinical translation remains limited by interindividual variability, methodological heterogeneity, and insufficient longitudinal evidence. Future efforts should focus on standardization, validation of microbiome-based biomarkers, and integration of multi-omics and artificial intelligence approaches to enable clinically actionable applications.
Additional Links: PMID-42171841
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@article {pmid42171841,
year = {2026},
author = {Gómez-Montañez, E and Rojas-Salazar, YL and Rojas-Salazar, JG},
title = {Microbiome in Gastrointestinal Tumors: Implications in Oncogenesis and Therapeutic Response : Microbiome in Gastrointestinal Tumors.},
journal = {Current oncology reports},
volume = {28},
number = {1},
pages = {},
pmid = {42171841},
issn = {1534-6269},
mesh = {Humans ; *Gastrointestinal Neoplasms/microbiology/therapy/pathology ; *Gastrointestinal Microbiome ; *Carcinogenesis ; *Dysbiosis/microbiology ; Tumor Microenvironment ; *Microbiota ; },
abstract = {PURPOSE OF REVIEW: To provide an updated overview of the role of the human microbiome in the initiation, progression, and therapeutic response of gastrointestinal tumors, emphasizing molecular, immunological, and metabolic mechanisms, as well as its potential as a target for novel therapeutic strategies.
RECENT FINDINGS: Emerging evidence demonstrates that microbiome dysbiosis contributes to carcinogenesis across gastrointestinal malignancies, including colorectal, gastric, hepatic, and pancreatic cancers. Microbial-derived metabolites, such as short-chain fatty acids and secondary bile acids, modulate key signaling pathways involved in cell proliferation, apoptosis, and genomic stability. In addition, the microbiome influences the tumor microenvironment and immune responses, shaping variability in treatment outcomes. Both preclinical and clinical studies have shown that microbiome composition affects the efficacy and toxicity of chemotherapy and immunotherapy. Notably, specific microbial signatures are being explored as non-invasive biomarkers for early detection and prognostic stratification, while microbiome modulation strategies, such as diet, probiotics, antibiotics, and fecal microbiota transplantation, have demonstrated potential to enhance therapeutic response. The bidirectional interaction between the microbiome and the host plays a central role in gastrointestinal tumorigenesis and treatment response. Although this field holds significant promise for precision oncology, its clinical translation remains limited by interindividual variability, methodological heterogeneity, and insufficient longitudinal evidence. Future efforts should focus on standardization, validation of microbiome-based biomarkers, and integration of multi-omics and artificial intelligence approaches to enable clinically actionable applications.},
}
MeSH Terms:
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Humans
*Gastrointestinal Neoplasms/microbiology/therapy/pathology
*Gastrointestinal Microbiome
*Carcinogenesis
*Dysbiosis/microbiology
Tumor Microenvironment
*Microbiota
RevDate: 2026-05-22
PathoFact 2.0: An Integrative Pipeline for the Prediction of Antimicrobial Resistance Genes, Virulence Factors, Toxins and Toxin-associated Proteins, and Biosynthetic Gene Clusters in Metagenomes.
GigaScience pii:8690703 [Epub ahead of print].
BACKGROUND: Antimicrobial resistance genes (ARG) and virulence factors (VFs) are central contributors to the global health crisis surrounding drug-resistant infections.
FINDINGS: We introduce PathoFact 2.0, an enhanced pipeline for improved ARG, VF, toxin, and biosynthetic gene clusters (BGC) prediction. Key improvements include an updated machine learning (ML) model for VF identification, expanded hidden Markov model profiles for VFs and toxin-associated proteins, a new ML model for toxin and toxin-associated proteins identification, and the integration of antiSMASH 7.0 for predicting biosynthetic gene clusters.
CONCLUSIONS: Our upgrades make PathoFact 2.0 a more powerful and user-friendly platform for predicting microbiome-based pathogenicity and resistance, providing a crucial tool for better understanding and addressing the challenges posed by antimicrobial resistance and infectious diseases.PathoFact 2.0 is available at https://gitlab.com/uniluxembourg/lcsb/systems-ecology/pathofact2. It is compatible with Linux operating systems.
Additional Links: PMID-42172047
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@article {pmid42172047,
year = {2026},
author = {Delgado, LF and Sunyer, JO and Laczny, CC and Hickl, O and May, P and Wilmes, P},
title = {PathoFact 2.0: An Integrative Pipeline for the Prediction of Antimicrobial Resistance Genes, Virulence Factors, Toxins and Toxin-associated Proteins, and Biosynthetic Gene Clusters in Metagenomes.},
journal = {GigaScience},
volume = {},
number = {},
pages = {},
doi = {10.1093/gigascience/giag062},
pmid = {42172047},
issn = {2047-217X},
abstract = {BACKGROUND: Antimicrobial resistance genes (ARG) and virulence factors (VFs) are central contributors to the global health crisis surrounding drug-resistant infections.
FINDINGS: We introduce PathoFact 2.0, an enhanced pipeline for improved ARG, VF, toxin, and biosynthetic gene clusters (BGC) prediction. Key improvements include an updated machine learning (ML) model for VF identification, expanded hidden Markov model profiles for VFs and toxin-associated proteins, a new ML model for toxin and toxin-associated proteins identification, and the integration of antiSMASH 7.0 for predicting biosynthetic gene clusters.
CONCLUSIONS: Our upgrades make PathoFact 2.0 a more powerful and user-friendly platform for predicting microbiome-based pathogenicity and resistance, providing a crucial tool for better understanding and addressing the challenges posed by antimicrobial resistance and infectious diseases.PathoFact 2.0 is available at https://gitlab.com/uniluxembourg/lcsb/systems-ecology/pathofact2. It is compatible with Linux operating systems.},
}
RevDate: 2026-05-24
CmpDate: 2026-05-22
The human microbiome in cancer: Not just a sidekick anymore.
Genetics and molecular biology, 49Suppl 1(Suppl 1):e20250236.
The human microbiome is increasingly recognized as a dynamic element in cancer biology. Studies across breast, prostate, lung, colorectal, and cervical tumors reveal that microbial communities influence carcinogenesis, immune regulation, and treatment outcomes. When the balance of these microorganisms is altered, inflammation becomes chronic, metabolism is disrupted, and signaling pathways such as NF-κB, IL6-STAT3, and β-catenin are activated. Bacterial metabolites and genotoxins, including colibactin and bile acids, may damage DNA and reshape the epigenetic landscape. Distinct microbial profiles have been linked to prognosis and to patient responses to chemotherapy and immunotherapy. The presence of beneficial taxa, such as Akkermansia muciniphila and Ruminococcus, has been associated with improved response to immune checkpoint inhibitors. At the same time, antibiotic-induced depletion of gut microbiome can reduce therapeutic efficacy. Strategies that help restore microbial balance, including probiotics, dietary interventions, and fecal microbiota transplantation, are being explored as complementary therapies. Although methodological differences and contamination remain challenges, the growing body of evidence indicates that the microbiome is a measurable and modifiable component of tumor ecosystems with strong potential for diagnostic, prognostic, and therapeutic applications in precision oncology.
Additional Links: PMID-42172181
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@article {pmid42172181,
year = {2026},
author = {Gomes, JV and Ribeiro, SPO and Nascimento, GMCD and Santos, DOD and Paula, DJG and Lima, SCS and Simão, TA},
title = {The human microbiome in cancer: Not just a sidekick anymore.},
journal = {Genetics and molecular biology},
volume = {49Suppl 1},
number = {Suppl 1},
pages = {e20250236},
pmid = {42172181},
issn = {1415-4757},
abstract = {The human microbiome is increasingly recognized as a dynamic element in cancer biology. Studies across breast, prostate, lung, colorectal, and cervical tumors reveal that microbial communities influence carcinogenesis, immune regulation, and treatment outcomes. When the balance of these microorganisms is altered, inflammation becomes chronic, metabolism is disrupted, and signaling pathways such as NF-κB, IL6-STAT3, and β-catenin are activated. Bacterial metabolites and genotoxins, including colibactin and bile acids, may damage DNA and reshape the epigenetic landscape. Distinct microbial profiles have been linked to prognosis and to patient responses to chemotherapy and immunotherapy. The presence of beneficial taxa, such as Akkermansia muciniphila and Ruminococcus, has been associated with improved response to immune checkpoint inhibitors. At the same time, antibiotic-induced depletion of gut microbiome can reduce therapeutic efficacy. Strategies that help restore microbial balance, including probiotics, dietary interventions, and fecal microbiota transplantation, are being explored as complementary therapies. Although methodological differences and contamination remain challenges, the growing body of evidence indicates that the microbiome is a measurable and modifiable component of tumor ecosystems with strong potential for diagnostic, prognostic, and therapeutic applications in precision oncology.},
}
RevDate: 2026-05-22
Gut microbiota dysbiosis and osteoporosis: pathogenesis and novel intervention strategies.
Future microbiology [Epub ahead of print].
Osteoporosis represents a major global public health challenge, with current pharmacological treatment often limited by substantial side effects. Recent research identifies the gut-bone axis as a key regulatory pathway linking gut microbiota to bone metabolic homeostasis. This review synthesizes findings from PubMed, Web of Science, and Scopus (up to March 2026) to elucidate how gut microbiota dysbiosis drives osteoporosis pathogenesis through interconnected mechanisms: aberrant immune modulation, altered microbial metabolites, impaired nutrient absorption, endocrine disruption, and systemic inflammation stemming from intestinal barrier failure. Consequently, these pathways disrupt the delicate balance of bone remodeling. Based on these insights, we outline novel microbiota-targeted therapeutic strategies, including probiotics, prebiotics, fecal microbiota transplantation, natural bioactive compounds, traditional Chinese medicine, and nanomaterials. These interventions aim to prevent and manage osteoporosis by reshaping the intestinal microecology via multi-target modulation. Future endeavors should prioritize in-depth mechanistic exploration, personalized precision interventions, and enhanced clinical translation to integrate these strategies into comprehensive osteoporosis care frameworks.
Additional Links: PMID-42172659
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@article {pmid42172659,
year = {2026},
author = {Liu, C and Yin, X and Yuan, X},
title = {Gut microbiota dysbiosis and osteoporosis: pathogenesis and novel intervention strategies.},
journal = {Future microbiology},
volume = {},
number = {},
pages = {1-12},
doi = {10.1080/17460913.2026.2678122},
pmid = {42172659},
issn = {1746-0921},
abstract = {Osteoporosis represents a major global public health challenge, with current pharmacological treatment often limited by substantial side effects. Recent research identifies the gut-bone axis as a key regulatory pathway linking gut microbiota to bone metabolic homeostasis. This review synthesizes findings from PubMed, Web of Science, and Scopus (up to March 2026) to elucidate how gut microbiota dysbiosis drives osteoporosis pathogenesis through interconnected mechanisms: aberrant immune modulation, altered microbial metabolites, impaired nutrient absorption, endocrine disruption, and systemic inflammation stemming from intestinal barrier failure. Consequently, these pathways disrupt the delicate balance of bone remodeling. Based on these insights, we outline novel microbiota-targeted therapeutic strategies, including probiotics, prebiotics, fecal microbiota transplantation, natural bioactive compounds, traditional Chinese medicine, and nanomaterials. These interventions aim to prevent and manage osteoporosis by reshaping the intestinal microecology via multi-target modulation. Future endeavors should prioritize in-depth mechanistic exploration, personalized precision interventions, and enhanced clinical translation to integrate these strategies into comprehensive osteoporosis care frameworks.},
}
RevDate: 2026-05-22
The mechanism of rumen microorganisms regulating fatty acid and lipid metabolism in brown adipose tissue of sheep analyzed by multi-omics analysis.
Food chemistry, 519:149670 pii:S0308-8146(26)01828-5 [Epub ahead of print].
Brown Adipose Tissue (BAT), a thermogenic fat in mammals that consumes energy rather than storing it, possesses unique characteristics. This study sought to clarify the specific mechanism and role of mutton in lipid deposition and nutritional quality. Using gas chromatography, lipidomics, and 16S rRNA gene sequencing, researchers found that BAT exhibited more active lipid metabolism, accompanied by increased abundance of the Firmicutes and Proteobacteria phyla. This activity manifested as a rise in beneficial DHA and EPA levels, along with a significant accumulation of key active lipids, such as cardiolipin and phosphatidylcholine. Further WGCNA and HCA analysis demonstrated that phyla including Verrucomicrobiota, Firmicutes, and Proteobacteria collectively enhanced BAT's nutritional value by regulating the biosynthesis of unsaturated fatty acids. This research successfully constructed a preliminary multi-dimensional interaction network of lipids and fatty acids within the "fat-rumen axis", providing a new theoretical framework for the accurate improvement of mutton's nutritional value.
Additional Links: PMID-42172767
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@article {pmid42172767,
year = {2026},
author = {Jin, X and Wu, D and Tong, Y and Weng, S and Jiang, Y and Zhang, J},
title = {The mechanism of rumen microorganisms regulating fatty acid and lipid metabolism in brown adipose tissue of sheep analyzed by multi-omics analysis.},
journal = {Food chemistry},
volume = {519},
number = {},
pages = {149670},
doi = {10.1016/j.foodchem.2026.149670},
pmid = {42172767},
issn = {1873-7072},
abstract = {Brown Adipose Tissue (BAT), a thermogenic fat in mammals that consumes energy rather than storing it, possesses unique characteristics. This study sought to clarify the specific mechanism and role of mutton in lipid deposition and nutritional quality. Using gas chromatography, lipidomics, and 16S rRNA gene sequencing, researchers found that BAT exhibited more active lipid metabolism, accompanied by increased abundance of the Firmicutes and Proteobacteria phyla. This activity manifested as a rise in beneficial DHA and EPA levels, along with a significant accumulation of key active lipids, such as cardiolipin and phosphatidylcholine. Further WGCNA and HCA analysis demonstrated that phyla including Verrucomicrobiota, Firmicutes, and Proteobacteria collectively enhanced BAT's nutritional value by regulating the biosynthesis of unsaturated fatty acids. This research successfully constructed a preliminary multi-dimensional interaction network of lipids and fatty acids within the "fat-rumen axis", providing a new theoretical framework for the accurate improvement of mutton's nutritional value.},
}
RevDate: 2026-05-22
Multi-omics association analysis of the toxicity mechanism differences of typical veterinary antibiotics on tomatoes: From physiological inhibition to metabolic reprogramming.
Journal of hazardous materials, 513:142457 pii:S0304-3894(26)01435-4 [Epub ahead of print].
Widespread application of veterinary antibiotics is contaminating soil via animal feces, leading to uptake by plants and environmental damage. Currently, research on the toxicological mechanisms associated with various classes of antibiotics remains inadequate. Therefore, this study utilized tomato as the test species and selected three representative antibiotics-chlortetracycline (CTC), enrofloxacin (ENR), and tylosin (TYL)-to systematically evaluate their differential toxicity and associated metabolic mechanisms through 14 and 28 days exposure experiments. At the individual level, antibiotics significantly suppressed biomass accumulation and photosynthesis in tomato seedlings, the ENR exhibited maximum inhibition rates of 37.4% for fresh weight and 26.7% for plant height. In contrast, the CTC recorded peak values of 28% for leaf area and 25.1% for SPAD measurements. Furthermore, exposure to antibiotics induced oxidative stress in tomato seedlings, with SOD demonstrating its highest activation rate of 18.3% in the TYL. Within the rhizosphere microenvironment, there was a notable decrease in the abundance of the dominant phylum Bryobacter, which was accompanied by alterations in bacterial community structure, an increase in network complexity, and a reduction in modularity. Under antibiotic stress, microbial communities demonstrated distinct metabolic responses: enhanced lipid metabolism in CTC, elevated carbohydrate metabolism with ENR, and activated nucleotide metabolism associated with TYL. In summary, antibiotics present global ecological risks by inhibiting plant growth and disrupting the rhizosphere microbiome. The class-specific toxicity of these substances necessitates the implementation of targeted risk management strategies.
Additional Links: PMID-42172829
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@article {pmid42172829,
year = {2026},
author = {Yang, H and Xie, Y and Wang, H and Sun, H and Li, X and Yao, X and Ding, J and Wang, Q and Lv, H and Turner, BL and Sun, S and Wang, J},
title = {Multi-omics association analysis of the toxicity mechanism differences of typical veterinary antibiotics on tomatoes: From physiological inhibition to metabolic reprogramming.},
journal = {Journal of hazardous materials},
volume = {513},
number = {},
pages = {142457},
doi = {10.1016/j.jhazmat.2026.142457},
pmid = {42172829},
issn = {1873-3336},
abstract = {Widespread application of veterinary antibiotics is contaminating soil via animal feces, leading to uptake by plants and environmental damage. Currently, research on the toxicological mechanisms associated with various classes of antibiotics remains inadequate. Therefore, this study utilized tomato as the test species and selected three representative antibiotics-chlortetracycline (CTC), enrofloxacin (ENR), and tylosin (TYL)-to systematically evaluate their differential toxicity and associated metabolic mechanisms through 14 and 28 days exposure experiments. At the individual level, antibiotics significantly suppressed biomass accumulation and photosynthesis in tomato seedlings, the ENR exhibited maximum inhibition rates of 37.4% for fresh weight and 26.7% for plant height. In contrast, the CTC recorded peak values of 28% for leaf area and 25.1% for SPAD measurements. Furthermore, exposure to antibiotics induced oxidative stress in tomato seedlings, with SOD demonstrating its highest activation rate of 18.3% in the TYL. Within the rhizosphere microenvironment, there was a notable decrease in the abundance of the dominant phylum Bryobacter, which was accompanied by alterations in bacterial community structure, an increase in network complexity, and a reduction in modularity. Under antibiotic stress, microbial communities demonstrated distinct metabolic responses: enhanced lipid metabolism in CTC, elevated carbohydrate metabolism with ENR, and activated nucleotide metabolism associated with TYL. In summary, antibiotics present global ecological risks by inhibiting plant growth and disrupting the rhizosphere microbiome. The class-specific toxicity of these substances necessitates the implementation of targeted risk management strategies.},
}
RevDate: 2026-05-22
Parvimonas micra is a specifically enriched bacterium in advanced canine periodontal disease and its effects are ameliorated using ADSCs-exosomes.
Veterinary microbiology, 318:111078 pii:S0378-1135(26)00210-5 [Epub ahead of print].
Canine periodontitis is a prevalent chronic inflammatory disease, with its pathological progression closely associated with oral microbiome dysbiosis and dysregulated host immune responses. This study aimed to characterize oral microbiome changes across different stages of canine periodontitis, identify bacteria associated with advanced disease and evaluate the immunomodulatory potential of adipose-derived stem cell exosomes (ADSCs-exosomes). We analyzed pooled subgingival and supragingival plaque samples collected from multiple oral sites in 60 dogs with clinical stages S0-S4 using 16S rRNA sequencing, and performed in vitro cell assays, ADSCs-exosomes isolation and characterization. Alpha-diversity analysis showed that, in this cohort and under our pooled oral sampling design, advanced periodontitis was associated with increased community richness and altered evenness at the subject level, while beta-diversity analysis confirmed marked structural differences among study groups (R[2] = 0.161, P = 0.001). P. micra showed significantly higher abundance in severe periodontitis (S4) and was identified by linear discriminant analysis effect-size (LEfSe), random forest, and analysis of variance (ANOVA) analyses (linear discriminant analysis (LDA) > 3.5, P < 0.01), suggesting an association with advanced disease. In vitro, P. micra reduced canine macrophage cell (DH82) (P < 0.05) viability and promoted a pro-inflammatory phenotypes. ADSCs-exosomes were internalized by canine macrophages and significantly downregulated pro-inflammatory cytokines (IL-1β, IL-6, iNOS) and upregulated anti-inflammatory markers (Arg-1, CD163, and IL-10) (P < 0.05), thereby partially reversing the inflammatory imbalance induced by P. micra. Together, these findings identify P. micra as a candidate bacterium associated with advanced canine periodontitis and suggest that ADSCs-exosomes may have potential as a host-modulatory therapeutic strategy in this disease.
Additional Links: PMID-42172872
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@article {pmid42172872,
year = {2026},
author = {Yu, M and Wang, Z and Han, X and Ge, Y and Geng, Z and Wang, J and Wang, D and Lian, S},
title = {Parvimonas micra is a specifically enriched bacterium in advanced canine periodontal disease and its effects are ameliorated using ADSCs-exosomes.},
journal = {Veterinary microbiology},
volume = {318},
number = {},
pages = {111078},
doi = {10.1016/j.vetmic.2026.111078},
pmid = {42172872},
issn = {1873-2542},
abstract = {Canine periodontitis is a prevalent chronic inflammatory disease, with its pathological progression closely associated with oral microbiome dysbiosis and dysregulated host immune responses. This study aimed to characterize oral microbiome changes across different stages of canine periodontitis, identify bacteria associated with advanced disease and evaluate the immunomodulatory potential of adipose-derived stem cell exosomes (ADSCs-exosomes). We analyzed pooled subgingival and supragingival plaque samples collected from multiple oral sites in 60 dogs with clinical stages S0-S4 using 16S rRNA sequencing, and performed in vitro cell assays, ADSCs-exosomes isolation and characterization. Alpha-diversity analysis showed that, in this cohort and under our pooled oral sampling design, advanced periodontitis was associated with increased community richness and altered evenness at the subject level, while beta-diversity analysis confirmed marked structural differences among study groups (R[2] = 0.161, P = 0.001). P. micra showed significantly higher abundance in severe periodontitis (S4) and was identified by linear discriminant analysis effect-size (LEfSe), random forest, and analysis of variance (ANOVA) analyses (linear discriminant analysis (LDA) > 3.5, P < 0.01), suggesting an association with advanced disease. In vitro, P. micra reduced canine macrophage cell (DH82) (P < 0.05) viability and promoted a pro-inflammatory phenotypes. ADSCs-exosomes were internalized by canine macrophages and significantly downregulated pro-inflammatory cytokines (IL-1β, IL-6, iNOS) and upregulated anti-inflammatory markers (Arg-1, CD163, and IL-10) (P < 0.05), thereby partially reversing the inflammatory imbalance induced by P. micra. Together, these findings identify P. micra as a candidate bacterium associated with advanced canine periodontitis and suggest that ADSCs-exosomes may have potential as a host-modulatory therapeutic strategy in this disease.},
}
RevDate: 2026-05-22
Effect of menstrual cups on vaginal health, reproductive tract and urogenital infections: a systematic review and meta-analysis.
EBioMedicine, 128:106307 pii:S2352-3964(26)00189-1 [Epub ahead of print].
BACKGROUND: The menstrual cup is a device inserted into the vagina during menstruation to collect blood. Evidence of its effect on the vaginal microbiome and associations with laboratory-confirmed infections is limited. We compiled existing information to assess associations between menstrual cups and reproductive tract infections (RTIs), sexually transmitted infections (STIs), and the vaginal microbiome.
METHODS: We searched four databases (PubMed, CINAHL, Global Health, and Scopus, from inception to January 23, 2026) for trials or observational studies reporting on menstrual cup use and laboratory-confirmed RTIs, STIs and the vaginal microbiome. Study quality was assessed using the Cochrane Collaboration tool for trials and the Joanna Briggs Institute Critical Appraisal Checklist for Cohort Studies. Outcomes of interest between cup-users and users of alternative menstrual products (non-cup users) were compared using prevalence ratios (PR). Meta-analyses were conducted using fixed-effects models to generate pooled estimates. PROSPERO registration: CRD42024559595.
FINDINGS: Eleven studies involving 10,268 participants were included. Only three studies were considered of good quality. In two randomised controlled studies in Kenya, menstrual cups reduced the risk of STIs relative to non-cup users (adjusted PR [aPR] 0.74, 95% CI 0.60-0.91, p = 0.037, n = 695, I[2] = 0.0%). The association with bacterial vaginosis was 0.81 (aPR, 0.63-1.04, p = 0.0963, n = 695, I[2] = 0.0%). When combining observational and randomised studies, a protective effect on bacterial vaginosis persisted (PR 0.79, 95% CI 0.69-0.90, p = 0.0004, five studies, n = 2103, I[2] = 0.0%, 3 continents). One trial showed an association between menstrual cups and HSV-2 of 0.71 (aPR, 95% CI 0.50-1.01, p = 0.057, n = 1451). Optimal vaginal community state type-1 (CST-I) was more likely among cup users compared to non-cup users (PR 1.18, 1.10-1.27, p < 0.0001, n = 2639, 5 studies in Kenya and Europe). No increased infection risks were noted among menstrual cup users across the infections evaluated. Main limitations included the low number and quality of existing studies.
INTERPRETATION: Menstrual cups reduced the risk of STIs in Kenya. For bacterial vaginosis, the association was consistent with a protective effect and supportive for a healthy vaginal microbiome composition in studies from different geographies. These data strengthen evidence on the value of menstrual cups as a global multipurpose menstrual product solution.
FUNDING: UK-Medical Research Council, Medical Research Foundation, USA-National Institutes of Health; National Institute of Child Health and Human Development, and the Gates Foundation.
Additional Links: PMID-42172920
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@article {pmid42172920,
year = {2026},
author = {Maria van Eijk, A and Quinn-Savory, A and Zulaika, G and Skinner, A and Mason, L and Green, SJ and Phillips-Howard, PA and Mehta, SD},
title = {Effect of menstrual cups on vaginal health, reproductive tract and urogenital infections: a systematic review and meta-analysis.},
journal = {EBioMedicine},
volume = {128},
number = {},
pages = {106307},
doi = {10.1016/j.ebiom.2026.106307},
pmid = {42172920},
issn = {2352-3964},
abstract = {BACKGROUND: The menstrual cup is a device inserted into the vagina during menstruation to collect blood. Evidence of its effect on the vaginal microbiome and associations with laboratory-confirmed infections is limited. We compiled existing information to assess associations between menstrual cups and reproductive tract infections (RTIs), sexually transmitted infections (STIs), and the vaginal microbiome.
METHODS: We searched four databases (PubMed, CINAHL, Global Health, and Scopus, from inception to January 23, 2026) for trials or observational studies reporting on menstrual cup use and laboratory-confirmed RTIs, STIs and the vaginal microbiome. Study quality was assessed using the Cochrane Collaboration tool for trials and the Joanna Briggs Institute Critical Appraisal Checklist for Cohort Studies. Outcomes of interest between cup-users and users of alternative menstrual products (non-cup users) were compared using prevalence ratios (PR). Meta-analyses were conducted using fixed-effects models to generate pooled estimates. PROSPERO registration: CRD42024559595.
FINDINGS: Eleven studies involving 10,268 participants were included. Only three studies were considered of good quality. In two randomised controlled studies in Kenya, menstrual cups reduced the risk of STIs relative to non-cup users (adjusted PR [aPR] 0.74, 95% CI 0.60-0.91, p = 0.037, n = 695, I[2] = 0.0%). The association with bacterial vaginosis was 0.81 (aPR, 0.63-1.04, p = 0.0963, n = 695, I[2] = 0.0%). When combining observational and randomised studies, a protective effect on bacterial vaginosis persisted (PR 0.79, 95% CI 0.69-0.90, p = 0.0004, five studies, n = 2103, I[2] = 0.0%, 3 continents). One trial showed an association between menstrual cups and HSV-2 of 0.71 (aPR, 95% CI 0.50-1.01, p = 0.057, n = 1451). Optimal vaginal community state type-1 (CST-I) was more likely among cup users compared to non-cup users (PR 1.18, 1.10-1.27, p < 0.0001, n = 2639, 5 studies in Kenya and Europe). No increased infection risks were noted among menstrual cup users across the infections evaluated. Main limitations included the low number and quality of existing studies.
INTERPRETATION: Menstrual cups reduced the risk of STIs in Kenya. For bacterial vaginosis, the association was consistent with a protective effect and supportive for a healthy vaginal microbiome composition in studies from different geographies. These data strengthen evidence on the value of menstrual cups as a global multipurpose menstrual product solution.
FUNDING: UK-Medical Research Council, Medical Research Foundation, USA-National Institutes of Health; National Institute of Child Health and Human Development, and the Gates Foundation.},
}
RevDate: 2026-05-22
Trimethylamine-N-oxide (TMAO) in multiorgan disease: mechanisms, translational insights, and therapeutic opportunities.
Drug discovery today pii:S1359-6446(26)00108-X [Epub ahead of print].
Trimethylamine-N-oxide (TMAO), a gut microbe-derived metabolite, acts as a key mediator linking diet, microbial metabolism, and disease across multiple organs. Beyond cardiovascular and metabolic disorders, TMAO has also been implicated in a variety of pathological processes. It influences endothelial, immune, neuronal, and cancer cells, as well as platelets, through mechanisms including oxidative stress, inflammation, and organelle dysfunction. Systemic TMAO levels are influenced by hepatic metabolism, renal clearance, and hormonal factors, offering opportunities for targeted therapies. Approaches to reduce TMAO levels, including pharmacological inhibitors, dietary or microbiome-based interventions, and multiorgan strategies, could slow disease progression. Thus, TMAO shows promise as a diagnostic biomarker and therapeutic target, supporting avenues for drug discovery and precision medicine.
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@article {pmid42173308,
year = {2026},
author = {Kumar Samanthapudi, VS and Ostos Mendoza, KC and Puvvala, S and Kamma, S and Kotla, S},
title = {Trimethylamine-N-oxide (TMAO) in multiorgan disease: mechanisms, translational insights, and therapeutic opportunities.},
journal = {Drug discovery today},
volume = {},
number = {},
pages = {104703},
doi = {10.1016/j.drudis.2026.104703},
pmid = {42173308},
issn = {1878-5832},
abstract = {Trimethylamine-N-oxide (TMAO), a gut microbe-derived metabolite, acts as a key mediator linking diet, microbial metabolism, and disease across multiple organs. Beyond cardiovascular and metabolic disorders, TMAO has also been implicated in a variety of pathological processes. It influences endothelial, immune, neuronal, and cancer cells, as well as platelets, through mechanisms including oxidative stress, inflammation, and organelle dysfunction. Systemic TMAO levels are influenced by hepatic metabolism, renal clearance, and hormonal factors, offering opportunities for targeted therapies. Approaches to reduce TMAO levels, including pharmacological inhibitors, dietary or microbiome-based interventions, and multiorgan strategies, could slow disease progression. Thus, TMAO shows promise as a diagnostic biomarker and therapeutic target, supporting avenues for drug discovery and precision medicine.},
}
RevDate: 2026-05-22
Nutritional, Growth, and Microbiome Implications of Oral Immunotherapy: Unintended Consequences and Clinical Considerations.
Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology pii:S1081-1206(26)00228-0 [Epub ahead of print].
Food allergy management has changed significantly, with oral immunotherapy (OIT) emerging as a widely adopted strategy to increase reaction thresholds and reduce the risk of severe allergic reactions. Alongside its immunological effects, OIT has important implications for nutrition, growth, and the gut microbiome. Traditional management of food allergy relies on strict allergen avoidance, which may compromise dietary adequacy and growth, particularly in children avoiding nutrient-dense foods such as cow's milk and eggs. OIT offers an opportunity to reintroduce these foods in controlled amounts, potentially improving nutrient intake and supporting growth trajectories. Emerging evidence highlights the role of the gut microbiome in modulating immune tolerance. Microbial diversity, metabolite production, and early-life colonization patterns influence regulatory immune pathways and epithelial barrier integrity. During OIT, microbiome changes appear modest and variable, with some studies suggesting taxon-specific or functional shifts rather than global restructuring. Importantly, dietary factors, particularly the use of ultra-processed foods as dosing vehicles, may confound microbiome outcomes and influence treatment responses. From a nutritional perspective, OIT presents both opportunities and risks. While allergen reintroduction may improve protein and micronutrient intake, reliance on energy-dense masking foods may increase the risk of excessive calorie intake and suboptimal diet quality. Growth outcomes during OIT appear generally favorable, particularly in younger children and those with lower baseline growth. This article summarizes current evidence on OIT, focusing on its interactions with diet, growth, and the gut microbiome, and highlights the need for integrated, multidisciplinary approaches to optimize both clinical and nutritional outcomes.
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@article {pmid42173442,
year = {2026},
author = {Venter, C and Ryczaj, K and Hicks, AG and Mack, DP and O'Mahony, L and Smith, PK and Brough, HA},
title = {Nutritional, Growth, and Microbiome Implications of Oral Immunotherapy: Unintended Consequences and Clinical Considerations.},
journal = {Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.anai.2026.05.024},
pmid = {42173442},
issn = {1534-4436},
abstract = {Food allergy management has changed significantly, with oral immunotherapy (OIT) emerging as a widely adopted strategy to increase reaction thresholds and reduce the risk of severe allergic reactions. Alongside its immunological effects, OIT has important implications for nutrition, growth, and the gut microbiome. Traditional management of food allergy relies on strict allergen avoidance, which may compromise dietary adequacy and growth, particularly in children avoiding nutrient-dense foods such as cow's milk and eggs. OIT offers an opportunity to reintroduce these foods in controlled amounts, potentially improving nutrient intake and supporting growth trajectories. Emerging evidence highlights the role of the gut microbiome in modulating immune tolerance. Microbial diversity, metabolite production, and early-life colonization patterns influence regulatory immune pathways and epithelial barrier integrity. During OIT, microbiome changes appear modest and variable, with some studies suggesting taxon-specific or functional shifts rather than global restructuring. Importantly, dietary factors, particularly the use of ultra-processed foods as dosing vehicles, may confound microbiome outcomes and influence treatment responses. From a nutritional perspective, OIT presents both opportunities and risks. While allergen reintroduction may improve protein and micronutrient intake, reliance on energy-dense masking foods may increase the risk of excessive calorie intake and suboptimal diet quality. Growth outcomes during OIT appear generally favorable, particularly in younger children and those with lower baseline growth. This article summarizes current evidence on OIT, focusing on its interactions with diet, growth, and the gut microbiome, and highlights the need for integrated, multidisciplinary approaches to optimize both clinical and nutritional outcomes.},
}
RevDate: 2026-05-22
Promicrobial mucoadhesive micro-composites enable delivery of beneficial oral bacteria to restore and modulate oral biofilm communities.
Journal of controlled release : official journal of the Controlled Release Society pii:S0168-3659(26)00447-5 [Epub ahead of print].
Imbalances within the oral microbiome, composed of over 700 phylotypes, drive both local diseases, including periodontitis, and systemic conditions, such as rheumatoid arthritis and cardiovascular disease. Given the overuse of conventional antimicrobial agents to manage oral diseases and the relapsing nature associated with current intervention strategies, innovative promicrobial approaches to oral biofilm community restoration are needed. Importantly, there is a critical unmet clinical need for active restoration and sustained delivery of beneficial oral commensals rather than continued disruption of already-imbalanced communities. We have developed a promicrobial formulation encapsulating live, health-associated, oral bacteria within mucoadhesive micro-composites to promote the establishment of beneficial biofilms under simulated oral flow conditions. We encapsulated and characterised a five-species bioactive consortia of oral bacteria in alginate micro-composites, surface modified with poly-l-lysine to enhance their adhesion to artificial saliva-coated surfaces in vitro. Dissemination of the encapsulated bacteria from the micro-composites led to the formation of stable oral biofilms. Notably, biofilm composition could be modulated by altering the encapsulated bioactive composition, enabling a tailored and targeted pathway to biofilm restoration. Under representative saliva flow, delivery of bioactives following their bioencapsulation resulted in strong biofilm-forming capacity, even in the presence of pre-existing oral bacterial communities containing pathobionts, highlighting their potential clinical applications in dental biofilm bioengineering. In experiments designed to simulate periodontal pocket debridement, we observed immunomodulation following treatment with bioactive formulations and pathobiont reduction when Limosilactobacillus reuteri was also incorporated into the consortia. These findings establish a framework for using sustained-release encapsulated probiotics to modulate the oral microbiome, offering a paradigm shift towards biofilm-promoting therapies for oral healthcare and paving the way for oral microbiome transplantation.
Additional Links: PMID-42173447
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@article {pmid42173447,
year = {2026},
author = {Harvey, HJ and Corrigan, S and Baiocco, D and Zhang, Z and Iqbal, TH and Teughels, W and Chapple, I and Horniblow, RD},
title = {Promicrobial mucoadhesive micro-composites enable delivery of beneficial oral bacteria to restore and modulate oral biofilm communities.},
journal = {Journal of controlled release : official journal of the Controlled Release Society},
volume = {},
number = {},
pages = {115044},
doi = {10.1016/j.jconrel.2026.115044},
pmid = {42173447},
issn = {1873-4995},
abstract = {Imbalances within the oral microbiome, composed of over 700 phylotypes, drive both local diseases, including periodontitis, and systemic conditions, such as rheumatoid arthritis and cardiovascular disease. Given the overuse of conventional antimicrobial agents to manage oral diseases and the relapsing nature associated with current intervention strategies, innovative promicrobial approaches to oral biofilm community restoration are needed. Importantly, there is a critical unmet clinical need for active restoration and sustained delivery of beneficial oral commensals rather than continued disruption of already-imbalanced communities. We have developed a promicrobial formulation encapsulating live, health-associated, oral bacteria within mucoadhesive micro-composites to promote the establishment of beneficial biofilms under simulated oral flow conditions. We encapsulated and characterised a five-species bioactive consortia of oral bacteria in alginate micro-composites, surface modified with poly-l-lysine to enhance their adhesion to artificial saliva-coated surfaces in vitro. Dissemination of the encapsulated bacteria from the micro-composites led to the formation of stable oral biofilms. Notably, biofilm composition could be modulated by altering the encapsulated bioactive composition, enabling a tailored and targeted pathway to biofilm restoration. Under representative saliva flow, delivery of bioactives following their bioencapsulation resulted in strong biofilm-forming capacity, even in the presence of pre-existing oral bacterial communities containing pathobionts, highlighting their potential clinical applications in dental biofilm bioengineering. In experiments designed to simulate periodontal pocket debridement, we observed immunomodulation following treatment with bioactive formulations and pathobiont reduction when Limosilactobacillus reuteri was also incorporated into the consortia. These findings establish a framework for using sustained-release encapsulated probiotics to modulate the oral microbiome, offering a paradigm shift towards biofilm-promoting therapies for oral healthcare and paving the way for oral microbiome transplantation.},
}
RevDate: 2026-05-22
CmpDate: 2026-05-22
Artificial intelligence in multi-omics analysis of gastrointestinal diseases.
Progress in molecular biology and translational science, 222:111-128.
The assessment and treatment of gastrointestinal diseases face numerous obstacles, including inadequate diagnostic methods, limited therapeutic alternatives, and unequal access to medical services across different regions. However, advancements in technology such as artificial intelligence, personalized medicine, and microbiome analysis offer promising avenues to address these difficulties. An interdisciplinary and patient-centered approach can significantly improve health outcomes and reduce the overall impact of these conditions on both patients and healthcare systems. To effectively utilize AI while safeguarding patient interests, it is essential to establish ethical standards, adopt patient-oriented regulations, and provide strong support structures for spreading awareness among both healthcare providers and recipients.
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@article {pmid42173626,
year = {2026},
author = {Sarkar, D},
title = {Artificial intelligence in multi-omics analysis of gastrointestinal diseases.},
journal = {Progress in molecular biology and translational science},
volume = {222},
number = {},
pages = {111-128},
doi = {10.1016/bs.pmbts.2026.02.003},
pmid = {42173626},
issn = {1878-0814},
mesh = {Humans ; *Artificial Intelligence ; *Gastrointestinal Diseases/genetics/microbiology/metabolism ; Precision Medicine ; *Genomics ; Multiomics ; },
abstract = {The assessment and treatment of gastrointestinal diseases face numerous obstacles, including inadequate diagnostic methods, limited therapeutic alternatives, and unequal access to medical services across different regions. However, advancements in technology such as artificial intelligence, personalized medicine, and microbiome analysis offer promising avenues to address these difficulties. An interdisciplinary and patient-centered approach can significantly improve health outcomes and reduce the overall impact of these conditions on both patients and healthcare systems. To effectively utilize AI while safeguarding patient interests, it is essential to establish ethical standards, adopt patient-oriented regulations, and provide strong support structures for spreading awareness among both healthcare providers and recipients.},
}
MeSH Terms:
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Humans
*Artificial Intelligence
*Gastrointestinal Diseases/genetics/microbiology/metabolism
Precision Medicine
*Genomics
Multiomics
RevDate: 2026-05-22
CmpDate: 2026-05-22
AI in multi-omics analysis in obstructive lung diseases.
Progress in molecular biology and translational science, 222:165-206.
The reports of obstructive lung diseases (OLDs) like asthma, chronic obstructive pulmonary disease (COPD), and bronchiectasis show increasing global prevalence. The available treatment options for these diseases are limited to antibiotics and steroids. Different multi-omics integration approaches have been applied in studying host, microbiome, and host-microbiome interactions in these diseases to get better insights. Artificial intelligence (AI)-based, as well as statistical and other approaches, are used for multi-omics analyses, specifically the integration of multi-omics data in OLDs. This chapter discusses various aspects of multi-omics integration studies in asthma, COPD, and bronchiectasis. Overall, these studies focused on disease subtype classification, risk assessment, association with genetic factors, and several other aspects.
Additional Links: PMID-42173629
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@article {pmid42173629,
year = {2026},
author = {Roy, P and Saha, S},
title = {AI in multi-omics analysis in obstructive lung diseases.},
journal = {Progress in molecular biology and translational science},
volume = {222},
number = {},
pages = {165-206},
doi = {10.1016/bs.pmbts.2026.01.025},
pmid = {42173629},
issn = {1878-0814},
mesh = {Humans ; *Artificial Intelligence ; *Lung Diseases, Obstructive/genetics/microbiology/metabolism ; Pulmonary Disease, Chronic Obstructive/genetics ; *Genomics ; Multiomics ; },
abstract = {The reports of obstructive lung diseases (OLDs) like asthma, chronic obstructive pulmonary disease (COPD), and bronchiectasis show increasing global prevalence. The available treatment options for these diseases are limited to antibiotics and steroids. Different multi-omics integration approaches have been applied in studying host, microbiome, and host-microbiome interactions in these diseases to get better insights. Artificial intelligence (AI)-based, as well as statistical and other approaches, are used for multi-omics analyses, specifically the integration of multi-omics data in OLDs. This chapter discusses various aspects of multi-omics integration studies in asthma, COPD, and bronchiectasis. Overall, these studies focused on disease subtype classification, risk assessment, association with genetic factors, and several other aspects.},
}
MeSH Terms:
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Humans
*Artificial Intelligence
*Lung Diseases, Obstructive/genetics/microbiology/metabolism
Pulmonary Disease, Chronic Obstructive/genetics
*Genomics
Multiomics
RevDate: 2026-05-22
CmpDate: 2026-05-22
Artificial intelligence-driven multi-omics analysis of gut-kidney axis in chronic kidney disease.
Progress in molecular biology and translational science, 222:85-110.
The complex interactions between gut microbiota and kidney function in chronic kidney disease (CKD) present a challenging phenomenon in nephrology research. This comprehensive review explores how artificial intelligence (AI) is utilised for our understanding of the gut-kidney axis through multiomics analysis, offering a new platform for disease management and therapeutic interventions. Recent advances in multi-omics technologies have generated unprecedented volumes of data across microbiomics, metabolomics and proteomics platforms, necessitating sophisticated AI-driven approaches for meaningful interpretation. So, we substantially examined how machine learning methods integrate the omics data to establish the relationship between the gut-kidney axis for a more accurate predictive model and biomarker discovery. In addition, we explained the overview of molecular routes that relate microbiome changes to uremic toxin generation and inflammatory cascades in CKD patients. This timely review offers significant basic insights into using AI to better understand the pathogenesis of CKD progression in early stages via the gut-kidney route.
Additional Links: PMID-42173637
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@article {pmid42173637,
year = {2026},
author = {Rajalakshmi, SG and Sreehari, E and Viswanathan, P},
title = {Artificial intelligence-driven multi-omics analysis of gut-kidney axis in chronic kidney disease.},
journal = {Progress in molecular biology and translational science},
volume = {222},
number = {},
pages = {85-110},
doi = {10.1016/bs.pmbts.2026.01.015},
pmid = {42173637},
issn = {1878-0814},
mesh = {*Renal Insufficiency, Chronic/microbiology/metabolism ; Humans ; *Artificial Intelligence ; *Gastrointestinal Microbiome ; *Kidney/metabolism/pathology ; Animals ; *Metabolomics ; Proteomics ; Multiomics ; },
abstract = {The complex interactions between gut microbiota and kidney function in chronic kidney disease (CKD) present a challenging phenomenon in nephrology research. This comprehensive review explores how artificial intelligence (AI) is utilised for our understanding of the gut-kidney axis through multiomics analysis, offering a new platform for disease management and therapeutic interventions. Recent advances in multi-omics technologies have generated unprecedented volumes of data across microbiomics, metabolomics and proteomics platforms, necessitating sophisticated AI-driven approaches for meaningful interpretation. So, we substantially examined how machine learning methods integrate the omics data to establish the relationship between the gut-kidney axis for a more accurate predictive model and biomarker discovery. In addition, we explained the overview of molecular routes that relate microbiome changes to uremic toxin generation and inflammatory cascades in CKD patients. This timely review offers significant basic insights into using AI to better understand the pathogenesis of CKD progression in early stages via the gut-kidney route.},
}
MeSH Terms:
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*Renal Insufficiency, Chronic/microbiology/metabolism
Humans
*Artificial Intelligence
*Gastrointestinal Microbiome
*Kidney/metabolism/pathology
Animals
*Metabolomics
Proteomics
Multiomics
RevDate: 2026-05-22
CmpDate: 2026-05-22
Staphylococcus aureus and Staphylococcus lugdunensis Act in Concert to Disrupt the Nasal Epithelial Barrier.
Clinical and translational allergy, 16(5):e70177.
INTRODUCTION: Chronic rhinosinusitis (CRS) pathophysiology and its link to microbiome is an area of ongoing investigation. Certain pathogens, in particular Staphylococcus aureus described to contribute to recalcitrant CRS. In addition, different species of coagulase negative staphylococci (CoNS) are frequently isolated from the sinonasal cavity of CRS patients. However, the influence of Staphylococcal species coexisting in the same niche on the inflammatory process remains unclear. The aim of this study was to explore the impact of exoproteins from various Staphylococcus species isolated from the same patients on the mucosal barrier.
METHODS: Staphylococcal species isolated from CRS and control patients were cultured from sinus swabs in planktonic and biofilm forms, and their exoproteins extracted. Primary human nasal epithelial cells (HNECs) from CRS patients were cultured at an air-liquid interface (ALI) and exposed to 20 μg/mL exoproteins or control. Barrier disruption and cytotoxicity were assessed by measuring the transepithelial electrical resistance (TEER), passage of fluorescein labeled dextrans and lactate dehydrogenase (LDH) levels. IL- 6 concentration was measured employing ELISA. Patient's matched sinonasal tissue samples were analyzed with flow cytometry to detect and quantify immune cells.
RESULTS: Forty-four Staphylococcal species were isolated from 22 CRS and control patients including: 22 S. aureus, 12 S. epidermidis, and 10 S. lugdunensis. 15 out of 22 S. aureus exoproteins significantly enhanced cytotoxicity, reduced TEER values and increased paracellular permeability compared to control (p < 0.05). By contrast, S. epidermidis and S. lugdunensis exoproteins caused either mild or negligible effects on the TEER values, cell viability, and paracellular permeability. However, S. lugdunensis exoproteins induced significantly higher IL-6 compared to control. Correlation analysis indicated S. aureus and S. lugdunensis from the same patient acted in concert to disrupt the nasal epithelial barrier and induce toxicity.
CONCLUSION: This study shows the significant and detrimental impact of the presence of S. aureus exoproteins on nasal epithelial cell barrier function. S. aureus and S. lugdunensis isolated from the same patients acted in concert to affect the nasal barrier and inducing toxicity.
Additional Links: PMID-42173692
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@article {pmid42173692,
year = {2026},
author = {Ambachew, S and Ramezanpour, M and Cooksley, CM and Shaghayegh, G and Burdon, I and Barry, EF and Fenix, KA and Wormald, PJ and Psaltis, AJ and Vreugde, S},
title = {Staphylococcus aureus and Staphylococcus lugdunensis Act in Concert to Disrupt the Nasal Epithelial Barrier.},
journal = {Clinical and translational allergy},
volume = {16},
number = {5},
pages = {e70177},
doi = {10.1002/clt2.70177},
pmid = {42173692},
issn = {2045-7022},
support = {Grant No. 0006008606//Australian National Health and Medical Research Council/ ; },
abstract = {INTRODUCTION: Chronic rhinosinusitis (CRS) pathophysiology and its link to microbiome is an area of ongoing investigation. Certain pathogens, in particular Staphylococcus aureus described to contribute to recalcitrant CRS. In addition, different species of coagulase negative staphylococci (CoNS) are frequently isolated from the sinonasal cavity of CRS patients. However, the influence of Staphylococcal species coexisting in the same niche on the inflammatory process remains unclear. The aim of this study was to explore the impact of exoproteins from various Staphylococcus species isolated from the same patients on the mucosal barrier.
METHODS: Staphylococcal species isolated from CRS and control patients were cultured from sinus swabs in planktonic and biofilm forms, and their exoproteins extracted. Primary human nasal epithelial cells (HNECs) from CRS patients were cultured at an air-liquid interface (ALI) and exposed to 20 μg/mL exoproteins or control. Barrier disruption and cytotoxicity were assessed by measuring the transepithelial electrical resistance (TEER), passage of fluorescein labeled dextrans and lactate dehydrogenase (LDH) levels. IL- 6 concentration was measured employing ELISA. Patient's matched sinonasal tissue samples were analyzed with flow cytometry to detect and quantify immune cells.
RESULTS: Forty-four Staphylococcal species were isolated from 22 CRS and control patients including: 22 S. aureus, 12 S. epidermidis, and 10 S. lugdunensis. 15 out of 22 S. aureus exoproteins significantly enhanced cytotoxicity, reduced TEER values and increased paracellular permeability compared to control (p < 0.05). By contrast, S. epidermidis and S. lugdunensis exoproteins caused either mild or negligible effects on the TEER values, cell viability, and paracellular permeability. However, S. lugdunensis exoproteins induced significantly higher IL-6 compared to control. Correlation analysis indicated S. aureus and S. lugdunensis from the same patient acted in concert to disrupt the nasal epithelial barrier and induce toxicity.
CONCLUSION: This study shows the significant and detrimental impact of the presence of S. aureus exoproteins on nasal epithelial cell barrier function. S. aureus and S. lugdunensis isolated from the same patients acted in concert to affect the nasal barrier and inducing toxicity.},
}
RevDate: 2026-05-22
CmpDate: 2026-05-22
Immune discrimination between commensals and pathogenic bacteria.
Virulence, 17(1):2677297.
Interaction with various bacteria is essential for the development of various components of the immune system. To prevent disease, the immune system must continuously discriminate between commensal and pathogenic bacteria. The immune system employs several mechanisms to discriminate between beneficial and harmful bacteria. This ensures selective immune tolerance toward commensals, especially in the gastrointestinal tract. Both commensal and pathogenic bacteria contain features that provoke immune responses. However, how the immune system reacts to or eliminates bacterial infections while preserving commensals is not fully understood. This review aims to explore the underlying mechanisms used by the immune system to distinguish between commensals and pathogenic bacteria. The review also addresses how commensals interact with immune system components to facilitate immune discrimination and host protection. Finally, dysbiosis and therapeutic interventions used to restore microbial balance are also discussed in this review.
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@article {pmid42173824,
year = {2026},
author = {Alanazi, HH},
title = {Immune discrimination between commensals and pathogenic bacteria.},
journal = {Virulence},
volume = {17},
number = {1},
pages = {2677297},
doi = {10.1080/21505594.2026.2677297},
pmid = {42173824},
issn = {2150-5608},
mesh = {Humans ; *Bacteria/immunology/pathogenicity ; *Symbiosis/immunology ; Gastrointestinal Microbiome/immunology ; Animals ; Dysbiosis/immunology/microbiology ; *Bacterial Infections/immunology/microbiology ; *Host-Pathogen Interactions/immunology ; Immune Tolerance ; *Bacterial Physiological Phenomena ; Gastrointestinal Tract/microbiology/immunology ; },
abstract = {Interaction with various bacteria is essential for the development of various components of the immune system. To prevent disease, the immune system must continuously discriminate between commensal and pathogenic bacteria. The immune system employs several mechanisms to discriminate between beneficial and harmful bacteria. This ensures selective immune tolerance toward commensals, especially in the gastrointestinal tract. Both commensal and pathogenic bacteria contain features that provoke immune responses. However, how the immune system reacts to or eliminates bacterial infections while preserving commensals is not fully understood. This review aims to explore the underlying mechanisms used by the immune system to distinguish between commensals and pathogenic bacteria. The review also addresses how commensals interact with immune system components to facilitate immune discrimination and host protection. Finally, dysbiosis and therapeutic interventions used to restore microbial balance are also discussed in this review.},
}
MeSH Terms:
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Humans
*Bacteria/immunology/pathogenicity
*Symbiosis/immunology
Gastrointestinal Microbiome/immunology
Animals
Dysbiosis/immunology/microbiology
*Bacterial Infections/immunology/microbiology
*Host-Pathogen Interactions/immunology
Immune Tolerance
*Bacterial Physiological Phenomena
Gastrointestinal Tract/microbiology/immunology
RevDate: 2026-05-22
Clinical significance of gut microbiota-derived metabolite trimethylamine N-oxide in patients with systemic lupus erythematosus.
Scientific reports pii:10.1038/s41598-026-53011-7 [Epub ahead of print].
Trimethylamine N-oxide (TMAO), a gut microbiota-derived metabolite, is associated with cardiovascular disease (CVD) via pro-inflammatory and pro-atherogenic mechanisms. Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with a significantly increased risk of CVD, however, the role of TMAO in SLE remains unclear. This study aimed to assess the clinical significance of TMAO in patients with SLE, including analyses of precursor metabolites and gut microbiome. A total of 207 participants were enrolled, including 157 patients with SLE and 50 healthy controls. Serum TMAO levels were measured using ELISA, fecal precursor metabolites including trimethylamine (TMA) were quantified by [1]H-NMR spectroscopy, and gut microbiota composition was assessed using 16S rRNA sequencing. SLE patients with CVD had significantly higher TMAO levels than HC (P = 0.028) and SLE patients without CVD (P = 0.004). Serum TMAO (P = 0.025) and fecal TMA (P = 0.032) levels were positively correlated with the Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) damage index. Serum TMAO was negatively correlated with steroid dose (P = 0.038). Distinct gut microbiota compositions were observed between SLE patients with and without CVD. TMAO is associated with cardiovascular disease and cumulative organ damage in SLE, potentially mediated by gut microbiome alterations and modulated by steroid therapy.
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@article {pmid42173935,
year = {2026},
author = {Yang, J and Park, Y and Jang, SG and Park, MJ and Moon, SJ and Choi, HK and Kwok, SK},
title = {Clinical significance of gut microbiota-derived metabolite trimethylamine N-oxide in patients with systemic lupus erythematosus.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-53011-7},
pmid = {42173935},
issn = {2045-2322},
support = {RS-2023-00224099//National Research Foundation of Korea/ ; },
abstract = {Trimethylamine N-oxide (TMAO), a gut microbiota-derived metabolite, is associated with cardiovascular disease (CVD) via pro-inflammatory and pro-atherogenic mechanisms. Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with a significantly increased risk of CVD, however, the role of TMAO in SLE remains unclear. This study aimed to assess the clinical significance of TMAO in patients with SLE, including analyses of precursor metabolites and gut microbiome. A total of 207 participants were enrolled, including 157 patients with SLE and 50 healthy controls. Serum TMAO levels were measured using ELISA, fecal precursor metabolites including trimethylamine (TMA) were quantified by [1]H-NMR spectroscopy, and gut microbiota composition was assessed using 16S rRNA sequencing. SLE patients with CVD had significantly higher TMAO levels than HC (P = 0.028) and SLE patients without CVD (P = 0.004). Serum TMAO (P = 0.025) and fecal TMA (P = 0.032) levels were positively correlated with the Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) damage index. Serum TMAO was negatively correlated with steroid dose (P = 0.038). Distinct gut microbiota compositions were observed between SLE patients with and without CVD. TMAO is associated with cardiovascular disease and cumulative organ damage in SLE, potentially mediated by gut microbiome alterations and modulated by steroid therapy.},
}
RevDate: 2026-05-22
Gut microbiota dysbiosis and altered fecal metabolome in patients with age-related cataract.
Scientific reports pii:10.1038/s41598-026-53261-5 [Epub ahead of print].
Age-related cataract (ARC) is a leading cause of vision loss with incompletely understood mechanisms. Emerging evidence suggests the gut microbiota can influence ocular health, yet the gut-eye connection in cataract remains unexplored. We characterized gut microbial communities and fecal metabolic profiles in 30 ARC patients and 30 healthy controls using 16S rDNA gene sequencing, untargeted LC-MS metabolomics, and targeted GC-MS for short-chain fatty acids (SCFAs). While alpha- and beta-diversity were comparable between groups, ARC patients exhibited significant dysbiosis, including reduced Gut Microbiome Health Index, increased Microbial Dysbiosis Index, higher relative abundance of Bifidobacterium and Klebsiella, and depletion of butyrate-producing taxa (Faecalibacterium, Clostridia). Fecal metabolomic profiles distinctly separated ARC patients from controls, with pathway analysis highlighting disruptions in glycerophospholipid and choline metabolism. Targeted analysis confirmed significant depletion of acetate, propionate, and butyrate in ARC patients (all P< 0.01), which positively correlated with beneficial genera abundance. This integrative study reveals that ARC patients harbor gut microbial dysbiosis and distinct fecal metabolomic signatures, notably a loss of SCFA-producing bacteria and anti-inflammatory SCFAs. These findings support a novel gut-eye axis in cataract pathogenesis and suggest that gut-derived microbial and metabolic biomarkers may aid in non-invasive risk assessment, while microbiome-targeted interventions could offer new preventive or therapeutic avenues.
Additional Links: PMID-42173975
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@article {pmid42173975,
year = {2026},
author = {Liu, Y and Sun, C and Liu, H and Shu, X and Yu, T and Gong, Y and Li, J},
title = {Gut microbiota dysbiosis and altered fecal metabolome in patients with age-related cataract.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-53261-5},
pmid = {42173975},
issn = {2045-2322},
support = {CSTB2022NSCQ-MSX1274//Natural Science Foundation Project of Chongqing, Chongqing Science and Technology Commission/ ; CSTB2023NSCQ-MSX0194//Natural Science Foundation Project of Chongqing, Chongqing Science and Technology Commission/ ; NSFC; 32300778//National Natural Science Foundation of China/ ; W015//CQMU Program for Youth Innovation in Future Medicine/ ; },
abstract = {Age-related cataract (ARC) is a leading cause of vision loss with incompletely understood mechanisms. Emerging evidence suggests the gut microbiota can influence ocular health, yet the gut-eye connection in cataract remains unexplored. We characterized gut microbial communities and fecal metabolic profiles in 30 ARC patients and 30 healthy controls using 16S rDNA gene sequencing, untargeted LC-MS metabolomics, and targeted GC-MS for short-chain fatty acids (SCFAs). While alpha- and beta-diversity were comparable between groups, ARC patients exhibited significant dysbiosis, including reduced Gut Microbiome Health Index, increased Microbial Dysbiosis Index, higher relative abundance of Bifidobacterium and Klebsiella, and depletion of butyrate-producing taxa (Faecalibacterium, Clostridia). Fecal metabolomic profiles distinctly separated ARC patients from controls, with pathway analysis highlighting disruptions in glycerophospholipid and choline metabolism. Targeted analysis confirmed significant depletion of acetate, propionate, and butyrate in ARC patients (all P< 0.01), which positively correlated with beneficial genera abundance. This integrative study reveals that ARC patients harbor gut microbial dysbiosis and distinct fecal metabolomic signatures, notably a loss of SCFA-producing bacteria and anti-inflammatory SCFAs. These findings support a novel gut-eye axis in cataract pathogenesis and suggest that gut-derived microbial and metabolic biomarkers may aid in non-invasive risk assessment, while microbiome-targeted interventions could offer new preventive or therapeutic avenues.},
}
RevDate: 2026-05-25
CmpDate: 2026-05-22
Changes in gut microbiota composition following water kefir consumption in healthy adults.
Scientific reports, 16(1):.
Fermented foods have gained increasing scientific interest for their potential to modulate gut microbiota and provide probiotic microorganisms with possible health benefits. This intervention trial examined the impact of daily consumption of water kefir, a sustainable plant-based fermented beverage, on gut microbiota composition in 40 healthy adults. Participants consumed 200 mL of homemade water kefir daily for 14 days, with fecal samples collected before and after the intervention. Some participants reported mild, transient gastrointestinal effects such as flatulence (32%) and bloating (24%), which are common when introducing live microorganisms, while others experienced reduced abdominal pain (28%), and most (66%) reported no noticeable change in symptoms. 16S rRNA sequencing revealed significant shifts in microbial composition, including a 6.5% decrease in Firmicutes and increases in Bacteroidetes (+ 21.6%) and Actinobacteria (+ 14.8%). At the species level, beneficial taxa such as Blautia spp. and Roseburia faecis increased, along with commensals including Bacteroides fragilis, Bacteroides uniformis, Gemmiger formicilis, Prevotella copri, and Parabacteroides distasonis (p < 0.01). Although α-diversity remained unchanged, β-diversity differed significantly between pre- and post-intervention samples (p = 0.025). By comparing the relative abundance of dominant genera in participants' gut microbiota and in water kefir, overlapping genera such as Lactobacillus, Bifidobacterium, Prevotella, Coprococcus, and Faecalibacterium were identified. Among these, Bifidobacterium and Prevotella increased, Coprococcus decreased, and Lactobacillus and Faecalibacterium remained stable. Genera exclusive to the gut microbiota also exhibited differential changes. These findings suggest that water kefir consumption is associated with modulation of the gut microbiota, including increases in saccharolytic and short-chain fatty acid (SCFA)-producing taxa, potentially influenced by its exopolysaccharides and microbial community. Some genera from water kefir may transiently affect the gut microbiome, and the concurrent increase in Bifidobacterium and Prevotella may suggest a potential probiotic-like effect. However, causality cannot be established, and further studies are needed to assess the persistence of these changes and their long-term clinical relevance.
Additional Links: PMID-42174008
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@article {pmid42174008,
year = {2026},
author = {de Mel, R and Al Khafaji, AH and Muthusamy, S and Xu, J and Håkansson, Å},
title = {Changes in gut microbiota composition following water kefir consumption in healthy adults.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {42174008},
issn = {2045-2322},
mesh = {Humans ; *Gastrointestinal Microbiome ; Adult ; Male ; *Kefir/microbiology ; Female ; Feces/microbiology ; RNA, Ribosomal, 16S/genetics ; Young Adult ; Healthy Volunteers ; Middle Aged ; Bacteria/genetics/classification/isolation & purification ; Water ; },
abstract = {Fermented foods have gained increasing scientific interest for their potential to modulate gut microbiota and provide probiotic microorganisms with possible health benefits. This intervention trial examined the impact of daily consumption of water kefir, a sustainable plant-based fermented beverage, on gut microbiota composition in 40 healthy adults. Participants consumed 200 mL of homemade water kefir daily for 14 days, with fecal samples collected before and after the intervention. Some participants reported mild, transient gastrointestinal effects such as flatulence (32%) and bloating (24%), which are common when introducing live microorganisms, while others experienced reduced abdominal pain (28%), and most (66%) reported no noticeable change in symptoms. 16S rRNA sequencing revealed significant shifts in microbial composition, including a 6.5% decrease in Firmicutes and increases in Bacteroidetes (+ 21.6%) and Actinobacteria (+ 14.8%). At the species level, beneficial taxa such as Blautia spp. and Roseburia faecis increased, along with commensals including Bacteroides fragilis, Bacteroides uniformis, Gemmiger formicilis, Prevotella copri, and Parabacteroides distasonis (p < 0.01). Although α-diversity remained unchanged, β-diversity differed significantly between pre- and post-intervention samples (p = 0.025). By comparing the relative abundance of dominant genera in participants' gut microbiota and in water kefir, overlapping genera such as Lactobacillus, Bifidobacterium, Prevotella, Coprococcus, and Faecalibacterium were identified. Among these, Bifidobacterium and Prevotella increased, Coprococcus decreased, and Lactobacillus and Faecalibacterium remained stable. Genera exclusive to the gut microbiota also exhibited differential changes. These findings suggest that water kefir consumption is associated with modulation of the gut microbiota, including increases in saccharolytic and short-chain fatty acid (SCFA)-producing taxa, potentially influenced by its exopolysaccharides and microbial community. Some genera from water kefir may transiently affect the gut microbiome, and the concurrent increase in Bifidobacterium and Prevotella may suggest a potential probiotic-like effect. However, causality cannot be established, and further studies are needed to assess the persistence of these changes and their long-term clinical relevance.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome
Adult
Male
*Kefir/microbiology
Female
Feces/microbiology
RNA, Ribosomal, 16S/genetics
Young Adult
Healthy Volunteers
Middle Aged
Bacteria/genetics/classification/isolation & purification
Water
RevDate: 2026-05-22
Spicy food intake and dietary factors shape the gut microbiome and metabolism of mucin and short-chain fatty acids in healthy adults.
Scientific reports pii:10.1038/s41598-026-53556-7 [Epub ahead of print].
Whether spicy food intake independently modulates mucin metabolism and short-chain fatty acid (SCFA) production or depends on co-ingested factors such as alcohol remains poorly understood. Herein, shotgun metagenomics characterized gut microbial composition, functional pathways, and their relationship with spicy food intake, alcohol consumption, and intestinal fatty acid-binding protein (I-FABP) and liver fatty acid-binding protein (L-FABP) levels in 229 healthy Korean adults. Alcohol intake was positively correlated with urinary I-FABP levels indicating mild epithelial stress, whereas spicy food intake was not associated with either FABP biomarker. Consumption of highly spicy foods resulted in increased abundance of SCFA-producing and mucin-metabolizing taxa, along with mucin degradation and SCFA production. Individuals with high alcohol intake showed stronger enrichment of mucin-degrading taxa with reduced SCFA flux and increased abundance of Proteobacteria and Fusobacteria. The cross-classified dietary groups exhibited distinct mucin and SCFA activity patterns. The Drink-High-Spicy-High (DHSH) group displayed elevated mucin turnover and SCFA production with dysbiosis. These findings suggest that spicy food may modulate mucus layer metabolism in a context-dependent manner, whereas alcohol more consistently perturbs mucin-SCFA networks and epithelial integrity.
Additional Links: PMID-42174021
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@article {pmid42174021,
year = {2026},
author = {Min, U and Kim, J and Kim, J and Jin, H and Oh, H and Ahn, S and Shin, H and Lee, W},
title = {Spicy food intake and dietary factors shape the gut microbiome and metabolism of mucin and short-chain fatty acids in healthy adults.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-53556-7},
pmid = {42174021},
issn = {2045-2322},
abstract = {Whether spicy food intake independently modulates mucin metabolism and short-chain fatty acid (SCFA) production or depends on co-ingested factors such as alcohol remains poorly understood. Herein, shotgun metagenomics characterized gut microbial composition, functional pathways, and their relationship with spicy food intake, alcohol consumption, and intestinal fatty acid-binding protein (I-FABP) and liver fatty acid-binding protein (L-FABP) levels in 229 healthy Korean adults. Alcohol intake was positively correlated with urinary I-FABP levels indicating mild epithelial stress, whereas spicy food intake was not associated with either FABP biomarker. Consumption of highly spicy foods resulted in increased abundance of SCFA-producing and mucin-metabolizing taxa, along with mucin degradation and SCFA production. Individuals with high alcohol intake showed stronger enrichment of mucin-degrading taxa with reduced SCFA flux and increased abundance of Proteobacteria and Fusobacteria. The cross-classified dietary groups exhibited distinct mucin and SCFA activity patterns. The Drink-High-Spicy-High (DHSH) group displayed elevated mucin turnover and SCFA production with dysbiosis. These findings suggest that spicy food may modulate mucus layer metabolism in a context-dependent manner, whereas alcohol more consistently perturbs mucin-SCFA networks and epithelial integrity.},
}
RevDate: 2026-05-22
Comment on "Gut microbiome impact on systemic therapy outcomes in metastatic renal cell carcinoma: a systematic review" by Gavi et al.
World journal of urology, 44(1):.
Additional Links: PMID-42174097
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@article {pmid42174097,
year = {2026},
author = {Ali, A},
title = {Comment on "Gut microbiome impact on systemic therapy outcomes in metastatic renal cell carcinoma: a systematic review" by Gavi et al.},
journal = {World journal of urology},
volume = {44},
number = {1},
pages = {},
pmid = {42174097},
issn = {1433-8726},
}
RevDate: 2026-05-22
Microbial Legacy: Mycobacterium vaccae ATCC 15483[T] intergenerationally diversifies the microbiome and enhances stress resilience in male mice.
Molecular psychiatry [Epub ahead of print].
According to the "Old Friends" hypothesis, the increased prevalence of stress-associated disorders in urban concrete landscapes of high-income countries is at least in part due to a reduced exposure to immunoregulatory microorganisms. The latter is particularly impactful when occurring during early prenatal and postnatal life. Accordingly, our own preclinical studies demonstrate that non-pathogenic rapid-growing mycobacteria, including Mycobacterium (M.) vaccae NCTC 11659 and M. vaccae ATCC 15483[T], have immunoregulatory and stress-protective effects when administered repeatedly prior to or during stressor exposure. Here, we advance these findings by showing that repeated intragastric (i.g.) administration of a heat-killed preparation of M. vaccae ATCC 15483[T] to female C57BL/6 N mice provides intergenerational stress protection. Their male offspring, despite never directly receiving administration of rapid-growing mycobacteria, were protected against multiple adverse consequences of chronic stress in adulthood. Moreover, correlational analyses implicate the fecal microbiome as a potential mediator of these effects, with M. vaccae ATCC 15483[T] intergenerationally facilitating α-diversity and increasing the relative abundance of bacterial taxa known to be potent short-chain fatty acid producers. Repeated intragastric (i.g.) administration of a heat-killed preparation of Mycobacterium (M.) vaccae ATCC 15483[T] (MvacATCC)vs. its vehicle borate-buffered saline (BBS) to adult nulliparous female C57BL/6N mice was intergenerationally protective against multiple negative physiological and immunological consequences of chronic subordinate colony housing (CSC; compared with respective single-housed control (SHC) mice), including adrenal hypertrophy, splenomegaly, thymus involution, and tibia growth reduction as well as increased splenic toll-like receptor (TLR) 2 and TLR4 protein concentrations and splenocyte ex vivo (re)activity, but also decreased splenic ex vivo glucocorticoid sensitivity, regulatory T cell (Treg) counts and Treg suppression capacity in their male offspring. In contrast, CSC-induced increase in splenic myeloid cell counts as well as of neutrophilic chemotactic activity was not affected intergenerationally by MvacATCC. Moreover, fecal microbiome analyses before and after CSC showed that MvacATCC intergenerationally facilitated α-diversity and relative abundance of bacterial taxa known to be potent short-chain fatty acid (SCFA) producers. Of note, we abstained from showing respective data of female offspring in the graphical abstract (*), as the intergenerational resilience effects of MvacATCC on female offspring were difficult to interpret. The latter was due to the fact that chronic adult stressor exposure (i.e., social instability paradigm, SIP) per se did not affect any of the physiological and immunological readouts reported in females. The graphical abstract was created with Biorender.com.
Additional Links: PMID-42174231
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@article {pmid42174231,
year = {2026},
author = {Schiele, J and Tsai, PL and Schimmele, T and Beck, S and Meyer, M and Mannes, M and Desmond, LW and Noschka, R and Huber-Lang, M and Haffner-Luntzer, M and Jarczok, MN and Lowry, CA and Reif, A and Langgartner, D and Stenger, S and Slattery, DA and Reber, SO},
title = {Microbial Legacy: Mycobacterium vaccae ATCC 15483[T] intergenerationally diversifies the microbiome and enhances stress resilience in male mice.},
journal = {Molecular psychiatry},
volume = {},
number = {},
pages = {},
pmid = {42174231},
issn = {1476-5578},
support = {RE 2911/ 23-1//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; German Research 251293561//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; German Research 251293561//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; SL 141/ 6-1//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; },
abstract = {According to the "Old Friends" hypothesis, the increased prevalence of stress-associated disorders in urban concrete landscapes of high-income countries is at least in part due to a reduced exposure to immunoregulatory microorganisms. The latter is particularly impactful when occurring during early prenatal and postnatal life. Accordingly, our own preclinical studies demonstrate that non-pathogenic rapid-growing mycobacteria, including Mycobacterium (M.) vaccae NCTC 11659 and M. vaccae ATCC 15483[T], have immunoregulatory and stress-protective effects when administered repeatedly prior to or during stressor exposure. Here, we advance these findings by showing that repeated intragastric (i.g.) administration of a heat-killed preparation of M. vaccae ATCC 15483[T] to female C57BL/6 N mice provides intergenerational stress protection. Their male offspring, despite never directly receiving administration of rapid-growing mycobacteria, were protected against multiple adverse consequences of chronic stress in adulthood. Moreover, correlational analyses implicate the fecal microbiome as a potential mediator of these effects, with M. vaccae ATCC 15483[T] intergenerationally facilitating α-diversity and increasing the relative abundance of bacterial taxa known to be potent short-chain fatty acid producers. Repeated intragastric (i.g.) administration of a heat-killed preparation of Mycobacterium (M.) vaccae ATCC 15483[T] (MvacATCC)vs. its vehicle borate-buffered saline (BBS) to adult nulliparous female C57BL/6N mice was intergenerationally protective against multiple negative physiological and immunological consequences of chronic subordinate colony housing (CSC; compared with respective single-housed control (SHC) mice), including adrenal hypertrophy, splenomegaly, thymus involution, and tibia growth reduction as well as increased splenic toll-like receptor (TLR) 2 and TLR4 protein concentrations and splenocyte ex vivo (re)activity, but also decreased splenic ex vivo glucocorticoid sensitivity, regulatory T cell (Treg) counts and Treg suppression capacity in their male offspring. In contrast, CSC-induced increase in splenic myeloid cell counts as well as of neutrophilic chemotactic activity was not affected intergenerationally by MvacATCC. Moreover, fecal microbiome analyses before and after CSC showed that MvacATCC intergenerationally facilitated α-diversity and relative abundance of bacterial taxa known to be potent short-chain fatty acid (SCFA) producers. Of note, we abstained from showing respective data of female offspring in the graphical abstract (*), as the intergenerational resilience effects of MvacATCC on female offspring were difficult to interpret. The latter was due to the fact that chronic adult stressor exposure (i.e., social instability paradigm, SIP) per se did not affect any of the physiological and immunological readouts reported in females. The graphical abstract was created with Biorender.com.},
}
RevDate: 2026-05-22
Habitat Type and Locality Structure the Midgut Microbiota of Aedes albopictus.
Microbial ecology pii:10.1007/s00248-026-02792-5 [Epub ahead of print].
The mosquito midgut microbiome plays a crucial role in nutrition, reproduction, and immunity, yet how locality and urban development shape these communities and their potential relevance to mosquito-pathogen interactions remains poorly understood. Here, we investigated bacterial community composition and diversity in the midguts of adult female Aedes albopictus collected from residential and woodland habitats of Champaign-Urbana and Charleston in Illinois, USA. We sequenced the V4 region of the 16 S rRNA gene from 160 samples and analyzed the data using QIIME 2. After quality and feature filtering, 112 samples were retained, yielding 2,531 unique amplicon sequence variants assigned to 34 bacterial phyla, 246 families, and 404 genera. Because formal contaminant assessment was not possible, findings should be interpreted with appropriate caution. Woodland habitats showed significantly higher Shannon diversity, observed ASV richness, and phylogenetic diversity than residential habitats, with Charleston woodland samples exhibiting the highest richness and phylogenetic diversity. Factorial analyses showed significant associations of both city and habitat type with Shannon diversity, observed richness, and Faith's phylogenetic diversity, with significant interaction terms also detected. Beta diversity analyses revealed distinct clustering of Charleston woodland samples, and factorial PERMANOVA indicated significant associations of both city and habitat type across all four beta diversity metrics, with the strongest interaction effect observed for unweighted UniFrac. In conclusion, these results show that habitat type and locality are strongly associated with the composition and diversity of the Ae. albopictus midgut microbiota, underscoring the importance of habitat-specific microbial patterns in mosquito biology.
Additional Links: PMID-42174303
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@article {pmid42174303,
year = {2026},
author = {Kim, CH and Ciloglu, A and Yan, J and Mackay, A and Noel, KR and Cooper, M and Oluoch, A and Canam, T and Stone, CM},
title = {Habitat Type and Locality Structure the Midgut Microbiota of Aedes albopictus.},
journal = {Microbial ecology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00248-026-02792-5},
pmid = {42174303},
issn = {1432-184X},
abstract = {The mosquito midgut microbiome plays a crucial role in nutrition, reproduction, and immunity, yet how locality and urban development shape these communities and their potential relevance to mosquito-pathogen interactions remains poorly understood. Here, we investigated bacterial community composition and diversity in the midguts of adult female Aedes albopictus collected from residential and woodland habitats of Champaign-Urbana and Charleston in Illinois, USA. We sequenced the V4 region of the 16 S rRNA gene from 160 samples and analyzed the data using QIIME 2. After quality and feature filtering, 112 samples were retained, yielding 2,531 unique amplicon sequence variants assigned to 34 bacterial phyla, 246 families, and 404 genera. Because formal contaminant assessment was not possible, findings should be interpreted with appropriate caution. Woodland habitats showed significantly higher Shannon diversity, observed ASV richness, and phylogenetic diversity than residential habitats, with Charleston woodland samples exhibiting the highest richness and phylogenetic diversity. Factorial analyses showed significant associations of both city and habitat type with Shannon diversity, observed richness, and Faith's phylogenetic diversity, with significant interaction terms also detected. Beta diversity analyses revealed distinct clustering of Charleston woodland samples, and factorial PERMANOVA indicated significant associations of both city and habitat type across all four beta diversity metrics, with the strongest interaction effect observed for unweighted UniFrac. In conclusion, these results show that habitat type and locality are strongly associated with the composition and diversity of the Ae. albopictus midgut microbiota, underscoring the importance of habitat-specific microbial patterns in mosquito biology.},
}
RevDate: 2026-05-22
CmpDate: 2026-05-22
Tryptophan Metabolism at the Crossroads of Immunity, Barrier Function, and the Microbiome in Atopic Dermatitis.
Clinical reviews in allergy & immunology, 69(1):.
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by complex interplay among immune imbalance, impaired barrier function, and alterations in host‒microbiome interactions. Accumulating evidence indicates that tryptophan (TRP) metabolism is associated with these core pathological processes. This review summarizes the major TRP metabolic pathways, including the kynurenine pathway, microbial indole production, and the serotonin-melatonin axis, and outlines how their respective metabolites influence cutaneous inflammation, immune regulation, and barrier integrity in the context of AD. We integrate findings from preclinical and clinical studies to describe disease-associated alterations in TRP metabolism in AD and their potential relevance to disease activity. In addition, we examine both existing and emerging therapeutic strategies aimed at correcting TRP metabolic imbalance, including pharmacological agents, dietary interventions, and probiotic supplementation. Overall, elucidating the multifaceted role of TRP metabolism in AD pathophysiology provides a rational foundation for developing more precise diagnostic tools and targeted therapeutic approaches.
Additional Links: PMID-42174322
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@article {pmid42174322,
year = {2026},
author = {Tan, Y and Peng, G and Abudouwanli, A and Zhao, W and Sun, Q and Yang, M and Ogawa, H and Okumura, K and Niyonsaba, F},
title = {Tryptophan Metabolism at the Crossroads of Immunity, Barrier Function, and the Microbiome in Atopic Dermatitis.},
journal = {Clinical reviews in allergy & immunology},
volume = {69},
number = {1},
pages = {},
pmid = {42174322},
issn = {1559-0267},
support = {24K23469//Japan Society for the Promotion of Science/ ; 24K11459//Japan Society for the Promotion of Science/ ; },
mesh = {Humans ; *Tryptophan/metabolism ; *Dermatitis, Atopic/metabolism/immunology/therapy/microbiology/etiology ; *Microbiota/immunology ; Animals ; *Skin/immunology/metabolism/microbiology ; Melatonin/metabolism ; Kynurenine/metabolism ; Immunity ; Probiotics/therapeutic use ; Serotonin/metabolism ; },
abstract = {Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by complex interplay among immune imbalance, impaired barrier function, and alterations in host‒microbiome interactions. Accumulating evidence indicates that tryptophan (TRP) metabolism is associated with these core pathological processes. This review summarizes the major TRP metabolic pathways, including the kynurenine pathway, microbial indole production, and the serotonin-melatonin axis, and outlines how their respective metabolites influence cutaneous inflammation, immune regulation, and barrier integrity in the context of AD. We integrate findings from preclinical and clinical studies to describe disease-associated alterations in TRP metabolism in AD and their potential relevance to disease activity. In addition, we examine both existing and emerging therapeutic strategies aimed at correcting TRP metabolic imbalance, including pharmacological agents, dietary interventions, and probiotic supplementation. Overall, elucidating the multifaceted role of TRP metabolism in AD pathophysiology provides a rational foundation for developing more precise diagnostic tools and targeted therapeutic approaches.},
}
MeSH Terms:
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Humans
*Tryptophan/metabolism
*Dermatitis, Atopic/metabolism/immunology/therapy/microbiology/etiology
*Microbiota/immunology
Animals
*Skin/immunology/metabolism/microbiology
Melatonin/metabolism
Kynurenine/metabolism
Immunity
Probiotics/therapeutic use
Serotonin/metabolism
RevDate: 2026-05-23
Causal effects of oral microbiome traits on female reproductive diseases: a two-sample Mendelian randomization study.
BMC women's health pii:10.1186/s12905-026-04547-3 [Epub ahead of print].
OBJECTIVE: Female reproductive diseases (FRDs) impose a substantial health burden. Observational studies suggest links between oral dysbiosis and systemic conditions, but whether oral microbial traits causally influence FRDs remains unclear. We used two-sample Mendelian randomization (MR) to evaluate potential causal effects of genetically predicted oral microbiome traits on FRDs.
METHODS: Genome-wide association study (GWAS) summary statistics for 44 salivary microbial traits were obtained from a publicly available oral microbiome GWAS based on the Danish ADDITION-PRO cohort (16 S rRNA profiling; European ancestry; n = 610). Outcome GWAS summary statistics for six FRDs were obtained from FinnGen (R12). The inverse-variance weighted (IVW) method was the primary analysis, complemented by MR-Egger, weighted median, and weighted mode. Sensitivity analyses included Cochran's Q, MR-Egger intercept, MR-PRESSO, leave-one-out, and Steiger directionality tests. Multiple testing for primary IVW analyses was addressed using Benjamini-Hochberg false discovery rate (FDR) correction.
RESULTS: In primary IVW analyses, several oral taxa showed nominal associations (P < 0.05) with uterine leiomyoma (class Bacilli: OR = 1.0303, 95% CI 1.0012-1.0602; genus Veillonella: OR = 1.0291, 95% CI 1.0075-1.0512) and tubal infertility (family Veillonellaceae: OR = 0.8640, 95% CI 0.7824-0.9541; genus Veillonella: OR = 0.8900, 95% CI 0.8167-0.9699). However, none of these associations remained statistically significant after Benjamini-Hochberg FDR correction for the primary IVW analyses (all q > 0.05). In sensitivity analyses, MR-PRESSO outlier correction suggested a nominal association between Rothia mucilaginosa and uterine leiomyoma (OR = 1.0228, 95% CI 1.0069-1.0391; P = 0.0202). Overall, sensitivity analyses and Steiger directionality tests did not indicate that the main signals were driven by strong directional pleiotropy or reverse causation.
CONCLUSION: This two-sample MR study provides suggestive, exploratory genetic evidence that specific oral microbiome traits may be linked to uterine leiomyoma and tubal infertility, but the evidence did not remain statistically significant after multiple-testing correction. Larger oral microbiome GWAS, independent outcome datasets, and functional studies are needed to validate these signals and clarify biological mechanisms.
Additional Links: PMID-42174554
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@article {pmid42174554,
year = {2026},
author = {Xing, X and Meng, W and Chen, W and Shi, X and Wei, D and Lu, Q},
title = {Causal effects of oral microbiome traits on female reproductive diseases: a two-sample Mendelian randomization study.},
journal = {BMC women's health},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12905-026-04547-3},
pmid = {42174554},
issn = {1472-6874},
support = {CYDXK202203//Multidisciplinary Clinical Research Innovation Team Project of Beijing Chao-Yang Hospital/ ; },
abstract = {OBJECTIVE: Female reproductive diseases (FRDs) impose a substantial health burden. Observational studies suggest links between oral dysbiosis and systemic conditions, but whether oral microbial traits causally influence FRDs remains unclear. We used two-sample Mendelian randomization (MR) to evaluate potential causal effects of genetically predicted oral microbiome traits on FRDs.
METHODS: Genome-wide association study (GWAS) summary statistics for 44 salivary microbial traits were obtained from a publicly available oral microbiome GWAS based on the Danish ADDITION-PRO cohort (16 S rRNA profiling; European ancestry; n = 610). Outcome GWAS summary statistics for six FRDs were obtained from FinnGen (R12). The inverse-variance weighted (IVW) method was the primary analysis, complemented by MR-Egger, weighted median, and weighted mode. Sensitivity analyses included Cochran's Q, MR-Egger intercept, MR-PRESSO, leave-one-out, and Steiger directionality tests. Multiple testing for primary IVW analyses was addressed using Benjamini-Hochberg false discovery rate (FDR) correction.
RESULTS: In primary IVW analyses, several oral taxa showed nominal associations (P < 0.05) with uterine leiomyoma (class Bacilli: OR = 1.0303, 95% CI 1.0012-1.0602; genus Veillonella: OR = 1.0291, 95% CI 1.0075-1.0512) and tubal infertility (family Veillonellaceae: OR = 0.8640, 95% CI 0.7824-0.9541; genus Veillonella: OR = 0.8900, 95% CI 0.8167-0.9699). However, none of these associations remained statistically significant after Benjamini-Hochberg FDR correction for the primary IVW analyses (all q > 0.05). In sensitivity analyses, MR-PRESSO outlier correction suggested a nominal association between Rothia mucilaginosa and uterine leiomyoma (OR = 1.0228, 95% CI 1.0069-1.0391; P = 0.0202). Overall, sensitivity analyses and Steiger directionality tests did not indicate that the main signals were driven by strong directional pleiotropy or reverse causation.
CONCLUSION: This two-sample MR study provides suggestive, exploratory genetic evidence that specific oral microbiome traits may be linked to uterine leiomyoma and tubal infertility, but the evidence did not remain statistically significant after multiple-testing correction. Larger oral microbiome GWAS, independent outcome datasets, and functional studies are needed to validate these signals and clarify biological mechanisms.},
}
RevDate: 2026-05-23
Seasonal particulate matter exposure is associated with upper respiratory microbiota restructuring in dairy heifers.
BMC veterinary research pii:10.1186/s12917-026-05580-y [Epub ahead of print].
BACKGROUND: Particulate matter (PM), particularly PM2.5 and PM10, is a major environmental health concern linked to respiratory diseases in humans and animals. Northern Thailand, especially Chiang Mai, experiences recurrent seasonal air pollution from biomass burning, exposing outdoor-housed livestock to elevated ambient PM levels. The bovine upper respiratory tract (URT) harbors both commensal and opportunistic microorganisms, and disruption of this microbiota may influence susceptibility to bovine respiratory disease (BRD). However, the impact of natural PM exposure on the bovine URT microbiota remains poorly understood.
RESULTS: Nasopharyngeal swabs from 25 clinically healthy dairy heifers were analyzed during low-PM and high-PM periods. During the high-PM period, peak PM2.5 levels exceeded 30 times the WHO 24-hour guideline. Alpha diversity, including observed features, Shannon diversity, and Simpson index, was significantly higher during the high-PM period than during the low-PM period. Beta diversity analysis showed significant differences in Bray-Curtis dissimilarity and Jaccard distance, indicating changes in both relative abundance-based community structure and presence-absence-based community membership. The high-PM period was characterized by altered taxonomic profiles, including higher proportions of Proteobacteria, Firmicutes, Gammaproteobacteria, and Bacilli, and lower proportions of Actinobacteriota, Bacteroidota, Actinobacteria, and Bacteroidia. Among selected dominant genera, Moraxella and Fusobacterium were significantly reduced during the high-PM period. BRD-associated genera, including Mycoplasma, Pasteurella, Mannheimia, and Histophilus, showed higher average relative abundances during the high-PM period; however, paired comparisons were not statistically significant.
CONCLUSIONS: Seasonal high-PM exposure in Chiang Mai was associated with measurable changes in the nasopharyngeal microbiota of clinically healthy dairy heifers, including increased alpha diversity, altered beta diversity, changes in taxonomic profiles, and reductions in selected dominant genera. These findings suggest that ambient air pollution may contribute to respiratory microbiota restructuring in dairy heifers. Further longitudinal studies integrating microbiota composition, host immune responses, farm-level environmental monitoring, and clinical respiratory outcomes are needed to clarify whether PM-associated microbiota changes contribute to BRD susceptibility.
Additional Links: PMID-42174615
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@article {pmid42174615,
year = {2026},
author = {Buddhasiri, S and Muangplod, T and Panathiwat, P and Chandrasrimuang, P and Jitjumnong, J and Boonyayatra, S and Singhla, T},
title = {Seasonal particulate matter exposure is associated with upper respiratory microbiota restructuring in dairy heifers.},
journal = {BMC veterinary research},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12917-026-05580-y},
pmid = {42174615},
issn = {1746-6148},
support = {R66IN00536, 2023//CMU Mid-Career Research Fellowship program, Chiang Mai University/ ; },
abstract = {BACKGROUND: Particulate matter (PM), particularly PM2.5 and PM10, is a major environmental health concern linked to respiratory diseases in humans and animals. Northern Thailand, especially Chiang Mai, experiences recurrent seasonal air pollution from biomass burning, exposing outdoor-housed livestock to elevated ambient PM levels. The bovine upper respiratory tract (URT) harbors both commensal and opportunistic microorganisms, and disruption of this microbiota may influence susceptibility to bovine respiratory disease (BRD). However, the impact of natural PM exposure on the bovine URT microbiota remains poorly understood.
RESULTS: Nasopharyngeal swabs from 25 clinically healthy dairy heifers were analyzed during low-PM and high-PM periods. During the high-PM period, peak PM2.5 levels exceeded 30 times the WHO 24-hour guideline. Alpha diversity, including observed features, Shannon diversity, and Simpson index, was significantly higher during the high-PM period than during the low-PM period. Beta diversity analysis showed significant differences in Bray-Curtis dissimilarity and Jaccard distance, indicating changes in both relative abundance-based community structure and presence-absence-based community membership. The high-PM period was characterized by altered taxonomic profiles, including higher proportions of Proteobacteria, Firmicutes, Gammaproteobacteria, and Bacilli, and lower proportions of Actinobacteriota, Bacteroidota, Actinobacteria, and Bacteroidia. Among selected dominant genera, Moraxella and Fusobacterium were significantly reduced during the high-PM period. BRD-associated genera, including Mycoplasma, Pasteurella, Mannheimia, and Histophilus, showed higher average relative abundances during the high-PM period; however, paired comparisons were not statistically significant.
CONCLUSIONS: Seasonal high-PM exposure in Chiang Mai was associated with measurable changes in the nasopharyngeal microbiota of clinically healthy dairy heifers, including increased alpha diversity, altered beta diversity, changes in taxonomic profiles, and reductions in selected dominant genera. These findings suggest that ambient air pollution may contribute to respiratory microbiota restructuring in dairy heifers. Further longitudinal studies integrating microbiota composition, host immune responses, farm-level environmental monitoring, and clinical respiratory outcomes are needed to clarify whether PM-associated microbiota changes contribute to BRD susceptibility.},
}
RevDate: 2026-05-23
Intratumoral microbiota exhibiting varied responses to neoadjuvant chemotherapy in triple-negative breast cancer revealed by 2bRAD-M.
Journal of translational medicine pii:10.1186/s12967-026-08187-x [Epub ahead of print].
BACKGROUND: Neoadjuvant chemotherapy (NACT) is the conventional therapy for early-stage and locally advanced triple-negative breast cancer (TNBC). Pathological complete response (pCR) serves as an essential indicator for predicting the effectiveness of NACT; however, a limited percentage of patients benefit from NACT. This research examined variations in the tumor microbiota between the pCR and non-pCR groups via 2BRAD sequencing for microbiome (2bRAD-M) technology and assessed the potential of the microbiota as a biomarker for predicting the NACT response.
METHODS: A total of 44 TNBC patients were enrolled, of whom 25 achieved pCR and 19 were classified as non-pCR patients. Clinical data were collected, tumor tissue was biopsied as sample, and DNA was extracted. The 2bRAD-M sequencing method was used to analyse the microbial communities and community structures of tumor tissues in both groups, conduct microbial diversity and differential analyses, and perform qualitative and quantitative studies on the microbes inside the tissues.
RESULTS: A total of 1,896 microbial species were identified. The microbial diversity in non-pCR tissue exceeded that in pCR patient tissue. The microbial composition of the tumor tissues in both groups was comparable. In the non-pCR group, there were significantly more gram-negative bacteria, such as Klebsiella, Escherichia, Acinetobacter, Vibrio, and Meiothermus, than in the pCR group. Calidithermus chliarophilus, Meiothermus sp.003226535, and Escherichia coli were identified as the three principal species distinguishing the two groups. Seven species were identified as markers to distinguish between non-pCRs and pCRs, with an AUC value of 90.3%. Validation in an independent cohort via qPCR indicated the potential predictive value of this seven-species model, yielding an AUC of 84%. Functional annotation analysis revealed 3,207 differentially expressed COGs and 230 differentially enriched signalling pathways across the non-pCR and pCR microbiomes. In vitro experiments suggested that lipopolysaccharide may contribute to doxorubicin and paclitaxel resistance in MDA-MB-231 cells, a process potentially linked to the reactivation of the PI3K/AKT signaling pathway.
CONCLUSION: This exploratory 2bRAD-M microbiome study of pCR and non-pCR tissues from TNBC patients receiving NACT identified significant differences in microbial environments between the two groups. Based on these findings, we developed a predictive model for chemotherapy effectiveness and highlighted the microbiome's potential as a biomarker for the efficacy of NACT in TNBC patients, offering novel insights that may inform future clinical diagnostic strategies.
Additional Links: PMID-42174668
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PubMed:
Citation:
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@article {pmid42174668,
year = {2026},
author = {Zhang, Z and Ma, X and Zhang, J and Wu, S and Zhang, X and Yang, C},
title = {Intratumoral microbiota exhibiting varied responses to neoadjuvant chemotherapy in triple-negative breast cancer revealed by 2bRAD-M.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-08187-x},
pmid = {42174668},
issn = {1479-5876},
abstract = {BACKGROUND: Neoadjuvant chemotherapy (NACT) is the conventional therapy for early-stage and locally advanced triple-negative breast cancer (TNBC). Pathological complete response (pCR) serves as an essential indicator for predicting the effectiveness of NACT; however, a limited percentage of patients benefit from NACT. This research examined variations in the tumor microbiota between the pCR and non-pCR groups via 2BRAD sequencing for microbiome (2bRAD-M) technology and assessed the potential of the microbiota as a biomarker for predicting the NACT response.
METHODS: A total of 44 TNBC patients were enrolled, of whom 25 achieved pCR and 19 were classified as non-pCR patients. Clinical data were collected, tumor tissue was biopsied as sample, and DNA was extracted. The 2bRAD-M sequencing method was used to analyse the microbial communities and community structures of tumor tissues in both groups, conduct microbial diversity and differential analyses, and perform qualitative and quantitative studies on the microbes inside the tissues.
RESULTS: A total of 1,896 microbial species were identified. The microbial diversity in non-pCR tissue exceeded that in pCR patient tissue. The microbial composition of the tumor tissues in both groups was comparable. In the non-pCR group, there were significantly more gram-negative bacteria, such as Klebsiella, Escherichia, Acinetobacter, Vibrio, and Meiothermus, than in the pCR group. Calidithermus chliarophilus, Meiothermus sp.003226535, and Escherichia coli were identified as the three principal species distinguishing the two groups. Seven species were identified as markers to distinguish between non-pCRs and pCRs, with an AUC value of 90.3%. Validation in an independent cohort via qPCR indicated the potential predictive value of this seven-species model, yielding an AUC of 84%. Functional annotation analysis revealed 3,207 differentially expressed COGs and 230 differentially enriched signalling pathways across the non-pCR and pCR microbiomes. In vitro experiments suggested that lipopolysaccharide may contribute to doxorubicin and paclitaxel resistance in MDA-MB-231 cells, a process potentially linked to the reactivation of the PI3K/AKT signaling pathway.
CONCLUSION: This exploratory 2bRAD-M microbiome study of pCR and non-pCR tissues from TNBC patients receiving NACT identified significant differences in microbial environments between the two groups. Based on these findings, we developed a predictive model for chemotherapy effectiveness and highlighted the microbiome's potential as a biomarker for the efficacy of NACT in TNBC patients, offering novel insights that may inform future clinical diagnostic strategies.},
}
RevDate: 2026-05-23
CmpDate: 2026-05-23
Effects of fecal microbiota transplantation and probiotics on the gut microbiome in antibiotic-treated septic patients: A pilot randomized controlled trial.
Virulence, 17(1):2668764.
Broad-spectrum antibiotics, essential for sepsis management in critically ill patients, cause significant gut dysbiosis. Restoring gut microbiota may improve outcomes, but the efficacy of interventions like fecal microbiota transplantation (FMT) and probiotics in this setting remains underexplored. This study aims to evaluate the feasibility and potential efficacy of FMT versus probiotics on gut microbiome restoration and inflammatory markers in critically ill, antibiotic-treated sepsis patients. In this single-center, prospective, exploratory pilot RCT, 40 sepsis patients were were randomized 2:1:1 to: Control (n = 20, antibiotics treatment), Probiotics (n = 10, antibiotics treatment combined one week of probiotics), and FMT (n = 10, antibiotics treatment combined one week of FMT) groups. Gut microbiota composition was analyzed using 16S rDNA sequencing, and clinical inflammatory markers were assessed at baseline, one week, and two weeks post-treatment. FMT significantly mitigated antibiotic-induced reductions in microbial diversity. At 2 weeks, the FMT group exhibited higher alpha-diversity (Chao1 index, p = 0.0125; Shannon/Simpson trends p = 0.06) compared to Control and Probiotics groups. FMT increased beneficial Bacteroides abundance and reduced Enterobacteriaceae. BugBase analysis revealed FMT significantly lowered pathogenic potential of gut microbiota (p = 0.021). Donor-recipient analysis showed FMT shifted recipient microbiomes toward donor enterotype. This study provides preliminary evidence that FMT, but not the probiotic regimen, effectively restores gut microbiome diversity and composition, reduces pathogenic potential, and may improve clinical outcomes in critically ill sepsis patients after broad-spectrum antibiotics. This study was registered on ClinicalTrials.gov (NCT05578196).
Additional Links: PMID-42174754
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PubMed:
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@article {pmid42174754,
year = {2026},
author = {Chen, Y and Zhao, J and Zhao, J and Chen, Q and Dong, S and Jia, S and Zhao, Y and Hao, D and Yin, Y and Lin, S and Chen, Y and Zhuang, Y and Peng, H},
title = {Effects of fecal microbiota transplantation and probiotics on the gut microbiome in antibiotic-treated septic patients: A pilot randomized controlled trial.},
journal = {Virulence},
volume = {17},
number = {1},
pages = {2668764},
doi = {10.1080/21505594.2026.2668764},
pmid = {42174754},
issn = {2150-5608},
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; *Probiotics/administration & dosage/therapeutic use ; *Fecal Microbiota Transplantation ; Pilot Projects ; Male ; Middle Aged ; Female ; *Sepsis/therapy/microbiology/drug therapy ; *Anti-Bacterial Agents/therapeutic use/adverse effects ; Aged ; Prospective Studies ; Critical Illness ; Dysbiosis/therapy ; Treatment Outcome ; Feces/microbiology ; Adult ; RNA, Ribosomal, 16S/genetics ; },
abstract = {Broad-spectrum antibiotics, essential for sepsis management in critically ill patients, cause significant gut dysbiosis. Restoring gut microbiota may improve outcomes, but the efficacy of interventions like fecal microbiota transplantation (FMT) and probiotics in this setting remains underexplored. This study aims to evaluate the feasibility and potential efficacy of FMT versus probiotics on gut microbiome restoration and inflammatory markers in critically ill, antibiotic-treated sepsis patients. In this single-center, prospective, exploratory pilot RCT, 40 sepsis patients were were randomized 2:1:1 to: Control (n = 20, antibiotics treatment), Probiotics (n = 10, antibiotics treatment combined one week of probiotics), and FMT (n = 10, antibiotics treatment combined one week of FMT) groups. Gut microbiota composition was analyzed using 16S rDNA sequencing, and clinical inflammatory markers were assessed at baseline, one week, and two weeks post-treatment. FMT significantly mitigated antibiotic-induced reductions in microbial diversity. At 2 weeks, the FMT group exhibited higher alpha-diversity (Chao1 index, p = 0.0125; Shannon/Simpson trends p = 0.06) compared to Control and Probiotics groups. FMT increased beneficial Bacteroides abundance and reduced Enterobacteriaceae. BugBase analysis revealed FMT significantly lowered pathogenic potential of gut microbiota (p = 0.021). Donor-recipient analysis showed FMT shifted recipient microbiomes toward donor enterotype. This study provides preliminary evidence that FMT, but not the probiotic regimen, effectively restores gut microbiome diversity and composition, reduces pathogenic potential, and may improve clinical outcomes in critically ill sepsis patients after broad-spectrum antibiotics. This study was registered on ClinicalTrials.gov (NCT05578196).},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/drug effects
*Probiotics/administration & dosage/therapeutic use
*Fecal Microbiota Transplantation
Pilot Projects
Male
Middle Aged
Female
*Sepsis/therapy/microbiology/drug therapy
*Anti-Bacterial Agents/therapeutic use/adverse effects
Aged
Prospective Studies
Critical Illness
Dysbiosis/therapy
Treatment Outcome
Feces/microbiology
Adult
RNA, Ribosomal, 16S/genetics
RevDate: 2026-05-23
CmpDate: 2026-05-23
Associations of bowel movements and stool types with risk of chronic kidney disease.
Medicine, 105(21):e48888.
The gut-kidney axis is increasingly recognized in chronic kidney disease (CKD) pathophysiology. Although stool frequency and consistency reflect gut microbiome status, their association with CKD remains underexplored. This study aimed to examine the relationship between bowel habits and CKD risk. In this cross-sectional analysis of 11,760 adults from National Health and Nutrition Examination Survey 2005 to 2010, stool frequency (weekly) and consistency (Bristol Stool Form Scale) were assessed. CKD was defined as estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73m2 and/or urine albumin-to-creatinine ratio (uACR) ≥ 30 mg/g. Weighted logistic regression adjusted for multiple confounders was used; subgroup and mediation analyses were performed. Diarrhea-like stool (Bristol Stool Form Scale types 6/7) was independently associated with higher CKD risk (odds ratio [OR] = 1.57, 95% confidence interval [CI]: 1.14-2.27), consistent across eGFR < 60 (OR = 1.42, 95% CI: 1.01-1.99) and uACR ≥ 30 mg/g (OR = 1.55, 95% CI: 1.03-2.23). Mediation analysis indicated that systemic inflammation (C-reactive protein) explained 10.1%, 8.5%, and 15.3% of these associations for eGFR decline, elevated uACR, and overall CKD, respectively. Subgroup analyses supported robustness across demographic and clinical strata. Bowel movement frequency was not significantly associated with CKD. Diarrhea-like stool consistency, partly mediated by systemic inflammation, is associated with increased CKD risk.
Additional Links: PMID-42175400
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@article {pmid42175400,
year = {2026},
author = {Wang, D and Zhang, F},
title = {Associations of bowel movements and stool types with risk of chronic kidney disease.},
journal = {Medicine},
volume = {105},
number = {21},
pages = {e48888},
doi = {10.1097/MD.0000000000048888},
pmid = {42175400},
issn = {1536-5964},
mesh = {Humans ; *Renal Insufficiency, Chronic/epidemiology/etiology/physiopathology ; Female ; Male ; Cross-Sectional Studies ; Middle Aged ; Glomerular Filtration Rate ; Adult ; Aged ; Risk Factors ; Nutrition Surveys ; *Feces ; *Defecation/physiology ; *Diarrhea/complications/epidemiology ; },
abstract = {The gut-kidney axis is increasingly recognized in chronic kidney disease (CKD) pathophysiology. Although stool frequency and consistency reflect gut microbiome status, their association with CKD remains underexplored. This study aimed to examine the relationship between bowel habits and CKD risk. In this cross-sectional analysis of 11,760 adults from National Health and Nutrition Examination Survey 2005 to 2010, stool frequency (weekly) and consistency (Bristol Stool Form Scale) were assessed. CKD was defined as estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73m2 and/or urine albumin-to-creatinine ratio (uACR) ≥ 30 mg/g. Weighted logistic regression adjusted for multiple confounders was used; subgroup and mediation analyses were performed. Diarrhea-like stool (Bristol Stool Form Scale types 6/7) was independently associated with higher CKD risk (odds ratio [OR] = 1.57, 95% confidence interval [CI]: 1.14-2.27), consistent across eGFR < 60 (OR = 1.42, 95% CI: 1.01-1.99) and uACR ≥ 30 mg/g (OR = 1.55, 95% CI: 1.03-2.23). Mediation analysis indicated that systemic inflammation (C-reactive protein) explained 10.1%, 8.5%, and 15.3% of these associations for eGFR decline, elevated uACR, and overall CKD, respectively. Subgroup analyses supported robustness across demographic and clinical strata. Bowel movement frequency was not significantly associated with CKD. Diarrhea-like stool consistency, partly mediated by systemic inflammation, is associated with increased CKD risk.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Renal Insufficiency, Chronic/epidemiology/etiology/physiopathology
Female
Male
Cross-Sectional Studies
Middle Aged
Glomerular Filtration Rate
Adult
Aged
Risk Factors
Nutrition Surveys
*Feces
*Defecation/physiology
*Diarrhea/complications/epidemiology
RevDate: 2026-05-23
CmpDate: 2026-05-23
The causal role of skin microbiota in rheumatoid arthritis via gut microbiota and immune cell mediation: A Mendelian randomization study.
Medicine, 105(21):e48847.
Emerging evidence suggests that disturbances in skin microbiota homeostasis may contribute to rheumatoid arthritis (RA) development through systemic immunomodulatory pathways. However, the causal relationships and underlying intermediary mechanisms remain to be clarified. We utilized summary-level data from large-scale genome-wide association studies and the FinnGen database, including 150 skin microbiota taxa, 731 immune cell phenotypes, 473 gut microbiota taxa, and RA cases. Two-sample Mendelian randomization (TSMR) was applied to evaluate potential causal associations with RA. Mediation analysis was further performed to identify the intermediary roles of immune cells and gut microbiota. Multiple sensitivity analyses were conducted to ensure the robustness of the findings. We identified significant causal associations between 6 skin microbiota, 25 immune cell phenotypes, and 19 gut microbiotas with RA. Mediation analysis indicated that certain immune cell traits and gut microbes may act as intermediaries in these relationships. Specifically, 20.3% of the protective effect of phylum Proteobacteria_Dry on RA risk was mediated by species Eubacterium F sp000434115. In contrast, genus Photobacterium accounted for 21.1% of the risk effect mediated by family Micrococcaceae_Dry. Additionally, immune phenotypes such as CD3+ Tregs and CX3CR1+ monocytes partially offset microbial risks, underscoring a novel "skin-gut-immune" axis in RA etiology. This Mendelian randomization study provides robust genetic evidence supporting the causal role of skin microbiota in rheumatoid arthritis pathogenesis via dual mediation pathways involving gut microbiota and immune cells. Our results suggest that targeting the skin and gut microbiota could represent a novel preventive or adjunctive therapeutic strategy for RA. For instance, probiotics or prebiotics aimed at enriching protective taxa (e.g., Proteobacteria, Fournierella massiliensis) or suppressing risk-associated microbes (e.g., Photobacterium, Brachyspira) might help restore immune homeostasis. Additionally, immunomodulatory approaches focusing on Treg enhancement or CX3CR1+ monocyte regulation could be informed by the identified immune phenotypes. Future studies should validate these mechanisms in longitudinal cohorts and explore microbiome-based precision medicine for RA.
Additional Links: PMID-42175487
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PubMed:
Citation:
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@article {pmid42175487,
year = {2026},
author = {Liu, D and Wu, L and Liu, X and Liu, Z and Kuang, L and Wu, S},
title = {The causal role of skin microbiota in rheumatoid arthritis via gut microbiota and immune cell mediation: A Mendelian randomization study.},
journal = {Medicine},
volume = {105},
number = {21},
pages = {e48847},
doi = {10.1097/MD.0000000000048847},
pmid = {42175487},
issn = {1536-5964},
support = {20231A010042, 20251A010040//Science and Technology Project of Guangzhou Municipal Health Commission/ ; 2023A03J0976, 2023A03J0492,2024A03J0499, 2025A03J3440//Science and Technology Program of Guangzhou City/ ; },
mesh = {Humans ; *Arthritis, Rheumatoid/immunology/microbiology/genetics ; Mendelian Randomization Analysis ; *Gastrointestinal Microbiome/immunology ; *Skin/microbiology/immunology ; *Microbiota/immunology ; Genome-Wide Association Study ; Skin Microbiome ; },
abstract = {Emerging evidence suggests that disturbances in skin microbiota homeostasis may contribute to rheumatoid arthritis (RA) development through systemic immunomodulatory pathways. However, the causal relationships and underlying intermediary mechanisms remain to be clarified. We utilized summary-level data from large-scale genome-wide association studies and the FinnGen database, including 150 skin microbiota taxa, 731 immune cell phenotypes, 473 gut microbiota taxa, and RA cases. Two-sample Mendelian randomization (TSMR) was applied to evaluate potential causal associations with RA. Mediation analysis was further performed to identify the intermediary roles of immune cells and gut microbiota. Multiple sensitivity analyses were conducted to ensure the robustness of the findings. We identified significant causal associations between 6 skin microbiota, 25 immune cell phenotypes, and 19 gut microbiotas with RA. Mediation analysis indicated that certain immune cell traits and gut microbes may act as intermediaries in these relationships. Specifically, 20.3% of the protective effect of phylum Proteobacteria_Dry on RA risk was mediated by species Eubacterium F sp000434115. In contrast, genus Photobacterium accounted for 21.1% of the risk effect mediated by family Micrococcaceae_Dry. Additionally, immune phenotypes such as CD3+ Tregs and CX3CR1+ monocytes partially offset microbial risks, underscoring a novel "skin-gut-immune" axis in RA etiology. This Mendelian randomization study provides robust genetic evidence supporting the causal role of skin microbiota in rheumatoid arthritis pathogenesis via dual mediation pathways involving gut microbiota and immune cells. Our results suggest that targeting the skin and gut microbiota could represent a novel preventive or adjunctive therapeutic strategy for RA. For instance, probiotics or prebiotics aimed at enriching protective taxa (e.g., Proteobacteria, Fournierella massiliensis) or suppressing risk-associated microbes (e.g., Photobacterium, Brachyspira) might help restore immune homeostasis. Additionally, immunomodulatory approaches focusing on Treg enhancement or CX3CR1+ monocyte regulation could be informed by the identified immune phenotypes. Future studies should validate these mechanisms in longitudinal cohorts and explore microbiome-based precision medicine for RA.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Arthritis, Rheumatoid/immunology/microbiology/genetics
Mendelian Randomization Analysis
*Gastrointestinal Microbiome/immunology
*Skin/microbiology/immunology
*Microbiota/immunology
Genome-Wide Association Study
Skin Microbiome
RevDate: 2026-05-23
CmpDate: 2026-05-23
Dietary patterns supportive of gut microbiota and bacterial vaginosis: A cross-sectional analysis from NHANES 2001 to 2004.
Medicine, 105(21):e48863.
Bacterial vaginosis (BV) is the leading form of vaginal microbiome imbalance in women of reproductive age and has been associated with dietary patterns and gut microbial profiles. This study investigated the association between a literature-based dietary index for gut microbiota (DI-GM) and BV prevalence in US women. We conducted a cross-sectional analysis of 1169 nonpregnant women aged 20 to 49 years from the National Health and Nutrition Examination Survey 2001 to 2004 with Nugent score measurements and complete dietary data. BV was defined as a Nugent score ≥ 7. Dietary intake was assessed via two 24-hour recalls, and DI-GM was computed based on 14 food groups classified as beneficial or unbeneficial for gut microbial health. Multivariable survey-weighted logistic regression models were used to estimate odds ratios and 95% confidence intervals. BV prevalence was 31.2%. Higher DI-GM scores were associated with lower odds of BV; women with scores ≥6 had reduced odds compared with those with scores of 0 to 3 (adjusted odds ratio = 0.75; 95% confidence interval: 0.60-0.94; P = .015; P-trend = .013). In conclusion, higher DI-GM scores were inversely associated with BV prevalence in this cross-sectional study. These findings should be interpreted cautiously, and prospective studies are needed to confirm causality.
Additional Links: PMID-42175520
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PubMed:
Citation:
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@article {pmid42175520,
year = {2026},
author = {Zeng, J and Ding, Z and Dai, Z},
title = {Dietary patterns supportive of gut microbiota and bacterial vaginosis: A cross-sectional analysis from NHANES 2001 to 2004.},
journal = {Medicine},
volume = {105},
number = {21},
pages = {e48863},
doi = {10.1097/MD.0000000000048863},
pmid = {42175520},
issn = {1536-5964},
mesh = {Humans ; Female ; Cross-Sectional Studies ; Adult ; *Vaginosis, Bacterial/epidemiology/microbiology ; Middle Aged ; Nutrition Surveys ; *Gastrointestinal Microbiome/physiology ; Young Adult ; Prevalence ; United States/epidemiology ; *Diet/statistics & numerical data ; },
abstract = {Bacterial vaginosis (BV) is the leading form of vaginal microbiome imbalance in women of reproductive age and has been associated with dietary patterns and gut microbial profiles. This study investigated the association between a literature-based dietary index for gut microbiota (DI-GM) and BV prevalence in US women. We conducted a cross-sectional analysis of 1169 nonpregnant women aged 20 to 49 years from the National Health and Nutrition Examination Survey 2001 to 2004 with Nugent score measurements and complete dietary data. BV was defined as a Nugent score ≥ 7. Dietary intake was assessed via two 24-hour recalls, and DI-GM was computed based on 14 food groups classified as beneficial or unbeneficial for gut microbial health. Multivariable survey-weighted logistic regression models were used to estimate odds ratios and 95% confidence intervals. BV prevalence was 31.2%. Higher DI-GM scores were associated with lower odds of BV; women with scores ≥6 had reduced odds compared with those with scores of 0 to 3 (adjusted odds ratio = 0.75; 95% confidence interval: 0.60-0.94; P = .015; P-trend = .013). In conclusion, higher DI-GM scores were inversely associated with BV prevalence in this cross-sectional study. These findings should be interpreted cautiously, and prospective studies are needed to confirm causality.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
Cross-Sectional Studies
Adult
*Vaginosis, Bacterial/epidemiology/microbiology
Middle Aged
Nutrition Surveys
*Gastrointestinal Microbiome/physiology
Young Adult
Prevalence
United States/epidemiology
*Diet/statistics & numerical data
RevDate: 2026-05-23
Salivary Microbiota From a Periodontitis Donor Is Associated With Altered IgA-Related Immune Features in Germ-Free Mice.
Journal of clinical periodontology [Epub ahead of print].
AIM: The oral microbiota has been implicated in mucosal immune regulation; however, its causal impact on salivary gland-associated immune features remains incompletely understood. In this proof-of-concept study, germ-free (GF) mice were colonised with salivary microbiota derived from either a periodontitis donor or a periodontally healthy donor, and IgA-associated immune readouts were evaluated across multiple compartments.
METHODS: GF mice were orally colonised with saliva-derived microbiota from a periodontitis patient or a periodontally healthy donor (or PBS). Total IgA in saliva, serum and faeces were quantified by ELISA. Cervical lymph nodes and blood were analysed by flow cytometry. Submandibular glands underwent histology and bulk RNA-seq.
RESULTS: Mice receiving microbiota from a periodontitis donor exhibited altered IgA levels in saliva, serum and faeces, increased faecal lipocalin-2, changes in innate immune cell distributions and increased CD138[+] cell signals and IgA immunoreactivity in the submandibular glands. Transcriptomic analysis revealed heterogeneous expression of individual IgA-related genes, with coordinated patterns observed at the level of IgA/mucosal defence-related gene sets.
CONCLUSIONS: These findings indicate that salivary microbiota from a periodontitis donor are associated with altered IgA-related immune features under GF conditions. While limited by the use of a single donor per group, this study provides proof-of-concept evidence supporting a potential role of oral microbiota in shaping salivary gland-associated immune characteristics.
Additional Links: PMID-42175662
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PubMed:
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@article {pmid42175662,
year = {2026},
author = {Irie, K and Azuma, T and Minoshima, R and Mochida, Y and Yamada, R and Nanashima, K and Fuchida, S and Kubota, N and Tsukinoki, K and Sato, Y and Tomofuji, T and Yamamoto, T},
title = {Salivary Microbiota From a Periodontitis Donor Is Associated With Altered IgA-Related Immune Features in Germ-Free Mice.},
journal = {Journal of clinical periodontology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jcpe.70146},
pmid = {42175662},
issn = {1600-051X},
support = {JP22K10316//JSPS KAKENHI/ ; JP25K13327//JSPS KAKENHI/ ; //Takeda Science Foundation/ ; },
abstract = {AIM: The oral microbiota has been implicated in mucosal immune regulation; however, its causal impact on salivary gland-associated immune features remains incompletely understood. In this proof-of-concept study, germ-free (GF) mice were colonised with salivary microbiota derived from either a periodontitis donor or a periodontally healthy donor, and IgA-associated immune readouts were evaluated across multiple compartments.
METHODS: GF mice were orally colonised with saliva-derived microbiota from a periodontitis patient or a periodontally healthy donor (or PBS). Total IgA in saliva, serum and faeces were quantified by ELISA. Cervical lymph nodes and blood were analysed by flow cytometry. Submandibular glands underwent histology and bulk RNA-seq.
RESULTS: Mice receiving microbiota from a periodontitis donor exhibited altered IgA levels in saliva, serum and faeces, increased faecal lipocalin-2, changes in innate immune cell distributions and increased CD138[+] cell signals and IgA immunoreactivity in the submandibular glands. Transcriptomic analysis revealed heterogeneous expression of individual IgA-related genes, with coordinated patterns observed at the level of IgA/mucosal defence-related gene sets.
CONCLUSIONS: These findings indicate that salivary microbiota from a periodontitis donor are associated with altered IgA-related immune features under GF conditions. While limited by the use of a single donor per group, this study provides proof-of-concept evidence supporting a potential role of oral microbiota in shaping salivary gland-associated immune characteristics.},
}
RevDate: 2026-05-23
CmpDate: 2026-05-23
Fecal Microbiome Varies With Social Group, Age and Bovine Tuberculosis Infection in the European Badger (Meles meles).
Molecular ecology, 35(10):e70369.
Host-associated microbes are key components of animal health and physiology, with particular importance for determining responses to pathogen infection. The gut microbiota is highly variable at the individual level, being shaped by a multitude of factors including diet, social behaviour, and age. Yet the relative influence of these traits on microbiota composition, and the consequences of this variation for host responses to pathogens remain unresolved. Here we investigate factors that shape the faecal microbiome in European badgers (Meles meles). Badgers act as a wildlife reservoir of Mycobacterium bovis, a zoonotic pathogen and the causative agent of bovine TB (bTB) in cattle, but the potential role of the microbiome in shaping patterns of infection and severity of disease is not known. Analysing 165 samples from 72 badgers over 3 years, we found that social group and age were key determinants of faecal microbiota composition and identified several bacterial genera associated with bTB infection. Investigation of microbiome dynamics at the individual level using longitudinally sampled badgers revealed marked heterogeneity in age-dependent microbiome trajectories that were not detectable from population level trends in chronological age. These data provide novel insights into the factors associated with microbial community dynamics in complex wild systems and highlight the need for individual-level and longitudinal approaches to studying host-microbiome associations.
Additional Links: PMID-42175702
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@article {pmid42175702,
year = {2026},
author = {Meadows, NML and Delahay, RJ and McDonald, RA and Powell, S and Hopkins, K and Arnold, L and Harrison, XA},
title = {Fecal Microbiome Varies With Social Group, Age and Bovine Tuberculosis Infection in the European Badger (Meles meles).},
journal = {Molecular ecology},
volume = {35},
number = {10},
pages = {e70369},
doi = {10.1111/mec.70369},
pmid = {42175702},
issn = {1365-294X},
support = {/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; },
mesh = {Animals ; *Mustelidae/microbiology ; *Feces/microbiology ; *Tuberculosis, Bovine/microbiology ; Cattle ; *Gastrointestinal Microbiome/genetics ; Age Factors ; Mycobacterium bovis/pathogenicity ; RNA, Ribosomal, 16S/genetics ; Social Behavior ; Social Group ; },
abstract = {Host-associated microbes are key components of animal health and physiology, with particular importance for determining responses to pathogen infection. The gut microbiota is highly variable at the individual level, being shaped by a multitude of factors including diet, social behaviour, and age. Yet the relative influence of these traits on microbiota composition, and the consequences of this variation for host responses to pathogens remain unresolved. Here we investigate factors that shape the faecal microbiome in European badgers (Meles meles). Badgers act as a wildlife reservoir of Mycobacterium bovis, a zoonotic pathogen and the causative agent of bovine TB (bTB) in cattle, but the potential role of the microbiome in shaping patterns of infection and severity of disease is not known. Analysing 165 samples from 72 badgers over 3 years, we found that social group and age were key determinants of faecal microbiota composition and identified several bacterial genera associated with bTB infection. Investigation of microbiome dynamics at the individual level using longitudinally sampled badgers revealed marked heterogeneity in age-dependent microbiome trajectories that were not detectable from population level trends in chronological age. These data provide novel insights into the factors associated with microbial community dynamics in complex wild systems and highlight the need for individual-level and longitudinal approaches to studying host-microbiome associations.},
}
MeSH Terms:
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hide MeSH Terms
Animals
*Mustelidae/microbiology
*Feces/microbiology
*Tuberculosis, Bovine/microbiology
Cattle
*Gastrointestinal Microbiome/genetics
Age Factors
Mycobacterium bovis/pathogenicity
RNA, Ribosomal, 16S/genetics
Social Behavior
Social Group
RevDate: 2026-05-23
Fluorogenic Coupled Assays Reveal Catalytic Properties, Inhibition Constants and Cellular Location of Mucin-Active Carbohydrate Sulfatases.
Angewandte Chemie (International ed. in English) [Epub ahead of print].
Sulfated glycans play a central role in human health and influence cell signaling, cancer progression, pathogen invasion, and host-microbiome interactions. Metabolism of these glycans requires a specialized class of enzymes termed carbohydrate sulfatases. These enzymes are particularly important in the human gut where sulfated colonic mucin is produced and subsequently degraded by colonic bacteria. Despite the biological importance of carbohydrate sulfatases, there is currently a lack of chemical tools to study their activity, substrate selectivity, inhibition, and the discovery of novel enzymes. To address this, we have synthesized new chemical tools to rapidly and quantitatively determine the activity and selectivity of carbohydrate sulfatases in plate-based coupled assays. We have synthesized 3-O-sulfated fluorogenic glycosides using efficient synthetic routes and combined these fluorogenic substrates with a glycosidase that selectively cleaves unsulfated glycosides, allowing sensitive detection of sulfatase activity on both purified protein and cell lysate from the S1_20 subfamily sulfatases. Furthermore, we show that the assay enables differentiation and quantification of substrate specificity, identification of sulfatase inhibitors, and determination of sulfatase (sub-)cellular location for two S1_20 subfamily sulfatases. Collectively, we anticipate that these tools will further our understanding of the interplay between carbohydrate sulfatases, sulfated glycans, and human health.
Additional Links: PMID-42175861
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@article {pmid42175861,
year = {2026},
author = {Tomlinson, CWE and Bergers, MD and Bolam, DN and Luis, AS and Cartmell, A and Armstrong, Z},
title = {Fluorogenic Coupled Assays Reveal Catalytic Properties, Inhibition Constants and Cellular Location of Mucin-Active Carbohydrate Sulfatases.},
journal = {Angewandte Chemie (International ed. in English)},
volume = {},
number = {},
pages = {e2991471},
doi = {10.1002/anie.2991471},
pmid = {42175861},
issn = {1521-3773},
support = {BB/T017805/1//BBSRC/ ; OCENW.M.24.135//NWO/ ; VI.Veni.212.173//NWO/ ; SBF005∖1065 163470//Academy of Medical Sciences/Wellcome Trust/ ; RGS∖R2∖212050//Royal Society/ ; 225897/Z/22/Z//Wellcome Trust CDA/ ; },
abstract = {Sulfated glycans play a central role in human health and influence cell signaling, cancer progression, pathogen invasion, and host-microbiome interactions. Metabolism of these glycans requires a specialized class of enzymes termed carbohydrate sulfatases. These enzymes are particularly important in the human gut where sulfated colonic mucin is produced and subsequently degraded by colonic bacteria. Despite the biological importance of carbohydrate sulfatases, there is currently a lack of chemical tools to study their activity, substrate selectivity, inhibition, and the discovery of novel enzymes. To address this, we have synthesized new chemical tools to rapidly and quantitatively determine the activity and selectivity of carbohydrate sulfatases in plate-based coupled assays. We have synthesized 3-O-sulfated fluorogenic glycosides using efficient synthetic routes and combined these fluorogenic substrates with a glycosidase that selectively cleaves unsulfated glycosides, allowing sensitive detection of sulfatase activity on both purified protein and cell lysate from the S1_20 subfamily sulfatases. Furthermore, we show that the assay enables differentiation and quantification of substrate specificity, identification of sulfatase inhibitors, and determination of sulfatase (sub-)cellular location for two S1_20 subfamily sulfatases. Collectively, we anticipate that these tools will further our understanding of the interplay between carbohydrate sulfatases, sulfated glycans, and human health.},
}
RevDate: 2026-05-23
CmpDate: 2026-05-23
Bacillus-derived antimicrobial peptides as alternatives to antibiotics in poultry: mechanisms, applications, and future prospects- a review.
Archives of microbiology, 208(8):.
Bacterial enteric pathogens, antimicrobial resistance, and mycotoxin-associated intestinal injury remain important challenges in poultry-associated systems. In this context, Bacillus-derived antimicrobial peptides (AMPs) have attracted attention as potential alternatives to conventional antibiotics due to their structural diversity and multifunctional properties. These peptides include ribosomally synthesized bacteriocins and non-ribosomally synthesized lipopeptides, such as surfactin, iturin, and fengycin. Their amphipathic structures enable interaction with microbial membranes, leading to permeabilization and disruption of cellular homeostasis. In addition to direct antimicrobial activity, these AMPs may interfere with biofilm-associated processes, modulate host immune responses, and help protect against toxin-induced epithelial injury. This review summarizes current knowledge on the diversity, structural characteristics, biosynthesis, mechanisms of action, and microbiological relevance of Bacillus AMPs in poultry-associated environments. Emphasis is placed on membrane targeting, biofilm regulation, immunomodulation, and mycotoxin-related gut protection, as well as limitations associated with antimicrobial resistance. Available evidence indicates that these peptides have diverse mechanisms of action; however, their activity is influenced by peptide class, formulation, microbial ecology, and host physiological factors. In addition, the potential for adaptive or genetically encoded resistance should be considered. Key translational challenges include peptide instability, variability in in vivo efficacy, strain-specific differences, safety considerations, and the lack of standardized comparative models. Future progress will depend on improved delivery systems, microbiome-resolved in vivo studies, and the integration of genomic mining, synthetic biology, and computational peptide design. These approaches may support the development of AMPs with improved stability, specificity, and functional performance in poultry-associated microbial systems.
Additional Links: PMID-42176025
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Citation:
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@article {pmid42176025,
year = {2026},
author = {Muhammad, N and Ansar, W and Bashir, T and Khan, HR},
title = {Bacillus-derived antimicrobial peptides as alternatives to antibiotics in poultry: mechanisms, applications, and future prospects- a review.},
journal = {Archives of microbiology},
volume = {208},
number = {8},
pages = {},
pmid = {42176025},
issn = {1432-072X},
mesh = {Animals ; *Antimicrobial Peptides/pharmacology/chemistry ; *Poultry/microbiology ; *Bacillus/chemistry/metabolism ; *Anti-Bacterial Agents/pharmacology ; Biofilms/drug effects ; *Poultry Diseases/microbiology/drug therapy ; },
abstract = {Bacterial enteric pathogens, antimicrobial resistance, and mycotoxin-associated intestinal injury remain important challenges in poultry-associated systems. In this context, Bacillus-derived antimicrobial peptides (AMPs) have attracted attention as potential alternatives to conventional antibiotics due to their structural diversity and multifunctional properties. These peptides include ribosomally synthesized bacteriocins and non-ribosomally synthesized lipopeptides, such as surfactin, iturin, and fengycin. Their amphipathic structures enable interaction with microbial membranes, leading to permeabilization and disruption of cellular homeostasis. In addition to direct antimicrobial activity, these AMPs may interfere with biofilm-associated processes, modulate host immune responses, and help protect against toxin-induced epithelial injury. This review summarizes current knowledge on the diversity, structural characteristics, biosynthesis, mechanisms of action, and microbiological relevance of Bacillus AMPs in poultry-associated environments. Emphasis is placed on membrane targeting, biofilm regulation, immunomodulation, and mycotoxin-related gut protection, as well as limitations associated with antimicrobial resistance. Available evidence indicates that these peptides have diverse mechanisms of action; however, their activity is influenced by peptide class, formulation, microbial ecology, and host physiological factors. In addition, the potential for adaptive or genetically encoded resistance should be considered. Key translational challenges include peptide instability, variability in in vivo efficacy, strain-specific differences, safety considerations, and the lack of standardized comparative models. Future progress will depend on improved delivery systems, microbiome-resolved in vivo studies, and the integration of genomic mining, synthetic biology, and computational peptide design. These approaches may support the development of AMPs with improved stability, specificity, and functional performance in poultry-associated microbial systems.},
}
MeSH Terms:
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Animals
*Antimicrobial Peptides/pharmacology/chemistry
*Poultry/microbiology
*Bacillus/chemistry/metabolism
*Anti-Bacterial Agents/pharmacology
Biofilms/drug effects
*Poultry Diseases/microbiology/drug therapy
RevDate: 2026-05-23
CmpDate: 2026-05-23
The Role of the Indoor Exposome in Food Allergy Development.
Current allergy and asthma reports, 26(1):.
PURPOSE OF REVIEW: Due to the rapid rise in the prevalence of food allergy, environmental exposures, in addition to genetic susceptibility, are likely contributors to allergic disease. In developed countries, individuals spend a substantial proportion of time indoors. Therefore, the indoor exposome provides a unique framework to examine factors driving the increase in the rates of food allergy. This review summarizes epidemiological and mechanistic evidence of the indoor exposome, consisting of the combined exposures to food antigens, microbes, and chemicals encountered in indoor environments during early life, and their influence on food allergy development.
RECENT FINDINGS: Indoor house dust contains detectable food allergens, which remain biologically active and may be linked to non-oral exposure, leading to allergic sensitization. In contrast, early-life exposures to diverse microbes and their products are associated with protection from allergic disease. Emerging evidence further demonstrates that indoor chemicals, including detergents, plasticizers, and pollutants, can disrupt epithelial barrier integrity or function as immune adjuvants, thus increasing susceptibility to food sensitization. Collectively, these findings highlight the indoor exposome as a complex and important determinant of food allergy risk. Improved understanding of how the indoor exposome influences food allergy development may inform future primary prevention or intervention strategies.
Additional Links: PMID-42176051
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Citation:
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@article {pmid42176051,
year = {2026},
author = {Humphrey, JR and Mathai, P and Moran, TP and Kulis, MD and Smeekens, JM},
title = {The Role of the Indoor Exposome in Food Allergy Development.},
journal = {Current allergy and asthma reports},
volume = {26},
number = {1},
pages = {},
pmid = {42176051},
issn = {1534-6315},
mesh = {Humans ; *Food Hypersensitivity/epidemiology/immunology/etiology ; *Allergens/immunology ; *Exposome ; *Environmental Exposure/adverse effects ; *Air Pollution, Indoor/adverse effects ; Animals ; },
abstract = {PURPOSE OF REVIEW: Due to the rapid rise in the prevalence of food allergy, environmental exposures, in addition to genetic susceptibility, are likely contributors to allergic disease. In developed countries, individuals spend a substantial proportion of time indoors. Therefore, the indoor exposome provides a unique framework to examine factors driving the increase in the rates of food allergy. This review summarizes epidemiological and mechanistic evidence of the indoor exposome, consisting of the combined exposures to food antigens, microbes, and chemicals encountered in indoor environments during early life, and their influence on food allergy development.
RECENT FINDINGS: Indoor house dust contains detectable food allergens, which remain biologically active and may be linked to non-oral exposure, leading to allergic sensitization. In contrast, early-life exposures to diverse microbes and their products are associated with protection from allergic disease. Emerging evidence further demonstrates that indoor chemicals, including detergents, plasticizers, and pollutants, can disrupt epithelial barrier integrity or function as immune adjuvants, thus increasing susceptibility to food sensitization. Collectively, these findings highlight the indoor exposome as a complex and important determinant of food allergy risk. Improved understanding of how the indoor exposome influences food allergy development may inform future primary prevention or intervention strategies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Food Hypersensitivity/epidemiology/immunology/etiology
*Allergens/immunology
*Exposome
*Environmental Exposure/adverse effects
*Air Pollution, Indoor/adverse effects
Animals
RevDate: 2026-05-23
CmpDate: 2026-05-23
Breakthroughs in HBV-related HCC Therapy: The Unmatched Potential of Immune Checkpoint Inhibitors.
Current treatment options in oncology, 27(1):.
Immune checkpoint inhibitors have reshaped the therapeutic landscape of hepatocellular carcinoma by restoring T cell-mediated antitumor immunity. However, the clinical benefit of monotherapy remains limited, highlighting the need for improved patient stratification and more effective treatment strategies. HBV-related hepatocellular carcinoma (HBV-HCC) is a major etiological subtype characterized by a chronically immunosuppressive tumor microenvironment driven by persistent viral antigen exposure and immune exhaustion. We believe that patients with HBV-HCC may be more suitable for immunotherapy, especially treatment with immune checkpoint inhibitors. A deeper understanding of the expression patterns of inhibitory checkpoint and costimulatory molecules, along with the identification of predictive biomarkers and the development of effective combination immunotherapies is essential for improving clinical outcomes. From a safety perspective, hepatitis B virus reactivation is generally manageable when appropriate antiviral therapy is administered concurrently with immunotherapy. Consequently, patients with HBV-HCC should not be excluded from treatment with immune checkpoint inhibitors. We anticipate that combination strategies, including multi-target immune checkpoint blockade, combinations with other immunotherapeutic approaches, and microbiome-based therapy, will further enhance therapeutic efficacy in HBV-HCC. Combination immune checkpoint therapy may enhance antitumor responses and potentially contribute to better control of viral activity.
Additional Links: PMID-42176073
PubMed:
Citation:
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@article {pmid42176073,
year = {2026},
author = {Liu, C and Chang, L and Yan, Y and Ji, H and Ma, J and Sun, H and Wang, L},
title = {Breakthroughs in HBV-related HCC Therapy: The Unmatched Potential of Immune Checkpoint Inhibitors.},
journal = {Current treatment options in oncology},
volume = {27},
number = {1},
pages = {},
pmid = {42176073},
issn = {1534-6277},
support = {2024ZD0523703//National Major Science and Technology Projects of China/ ; 2021-I2M-1-060//Chinese Academy of Medical Sciences/ ; BJ-2025-169//National High Level Hospital Clinical Research Funding/ ; },
mesh = {Humans ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; *Carcinoma, Hepatocellular/etiology/drug therapy/therapy/virology/pathology ; *Liver Neoplasms/etiology/drug therapy/therapy/virology ; *Hepatitis B virus/immunology ; Tumor Microenvironment/immunology/drug effects ; Immunotherapy/methods ; Combined Modality Therapy ; *Hepatitis B/complications/virology ; Treatment Outcome ; Disease Management ; },
abstract = {Immune checkpoint inhibitors have reshaped the therapeutic landscape of hepatocellular carcinoma by restoring T cell-mediated antitumor immunity. However, the clinical benefit of monotherapy remains limited, highlighting the need for improved patient stratification and more effective treatment strategies. HBV-related hepatocellular carcinoma (HBV-HCC) is a major etiological subtype characterized by a chronically immunosuppressive tumor microenvironment driven by persistent viral antigen exposure and immune exhaustion. We believe that patients with HBV-HCC may be more suitable for immunotherapy, especially treatment with immune checkpoint inhibitors. A deeper understanding of the expression patterns of inhibitory checkpoint and costimulatory molecules, along with the identification of predictive biomarkers and the development of effective combination immunotherapies is essential for improving clinical outcomes. From a safety perspective, hepatitis B virus reactivation is generally manageable when appropriate antiviral therapy is administered concurrently with immunotherapy. Consequently, patients with HBV-HCC should not be excluded from treatment with immune checkpoint inhibitors. We anticipate that combination strategies, including multi-target immune checkpoint blockade, combinations with other immunotherapeutic approaches, and microbiome-based therapy, will further enhance therapeutic efficacy in HBV-HCC. Combination immune checkpoint therapy may enhance antitumor responses and potentially contribute to better control of viral activity.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology
*Carcinoma, Hepatocellular/etiology/drug therapy/therapy/virology/pathology
*Liver Neoplasms/etiology/drug therapy/therapy/virology
*Hepatitis B virus/immunology
Tumor Microenvironment/immunology/drug effects
Immunotherapy/methods
Combined Modality Therapy
*Hepatitis B/complications/virology
Treatment Outcome
Disease Management
RevDate: 2026-05-23
CmpDate: 2026-05-23
MyBioScope: a new frontier in gut microbiome and health research.
Bioresources and bioprocessing, 13(1):.
UNLABELLED: Disruptions in the gut microbiome are linked to various diseases, but their roles in conditions such as age-related muscle loss (sarcopenia) and drug-induced microbial changes remain poorly understood. To address this gap, MyBioScope, a novel in vitro model using the DASbox[®] mini bioreactor system and human stool samples, was developed to simulate the anaerobic environment of the gastrointestinal (GI) tract. Bioreactors containing 120–200 mL of cultivation media were inoculated with stool slurry, stabilized over 24 h, and maintained with a customizable feeding protocol for multi-day experiments. Samples were analyzed using 16S rRNA gene sequencing, quantitative PCR, and metabolomics. Four pilot studies were conducted to validate the platform and model specific disease states, including proton pump inhibitor-induced GI tract oralization and microbiome alterations associated with sarcopenia. The workflow incorporated an anaerobic stool collection kit for user-friendly, room-temperature sample transport and storage. Our results demonstrated consistent microbial community structure and metabolic activity within disease-mimicking conditions. MyBioScope enabled reproducible, controlled studies of gut microbial dynamics and provided a scalable tool for investigating disease-specific microbiome changes. This platform may support translational efforts to integrate microbiome insights into clinical research, therapeutic development, and personalized medicine. In conclusion, this novel bioreactor-based in vitro model, MyBioScope, shows strong potential for in-depth exploration of disease-specific microbiomes and can facilitate new ways for integrating the knowledge of the microbiome’s impact on human health and disease into clinical practice.
GRAPHICAL ABSTRACT: [Image: see text]
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s40643-026-01044-1.
Additional Links: PMID-42176089
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Citation:
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@article {pmid42176089,
year = {2026},
author = {Žukauskaitė, K and Horvath, A and Tripolt, S and Habisch, H and Madl, T and Pacher-Deutsch, C and Nepel, M and Balazs, I and Stadlbauer, V},
title = {MyBioScope: a new frontier in gut microbiome and health research.},
journal = {Bioresources and bioprocessing},
volume = {13},
number = {1},
pages = {},
pmid = {42176089},
issn = {2197-4365},
abstract = {UNLABELLED: Disruptions in the gut microbiome are linked to various diseases, but their roles in conditions such as age-related muscle loss (sarcopenia) and drug-induced microbial changes remain poorly understood. To address this gap, MyBioScope, a novel in vitro model using the DASbox[®] mini bioreactor system and human stool samples, was developed to simulate the anaerobic environment of the gastrointestinal (GI) tract. Bioreactors containing 120–200 mL of cultivation media were inoculated with stool slurry, stabilized over 24 h, and maintained with a customizable feeding protocol for multi-day experiments. Samples were analyzed using 16S rRNA gene sequencing, quantitative PCR, and metabolomics. Four pilot studies were conducted to validate the platform and model specific disease states, including proton pump inhibitor-induced GI tract oralization and microbiome alterations associated with sarcopenia. The workflow incorporated an anaerobic stool collection kit for user-friendly, room-temperature sample transport and storage. Our results demonstrated consistent microbial community structure and metabolic activity within disease-mimicking conditions. MyBioScope enabled reproducible, controlled studies of gut microbial dynamics and provided a scalable tool for investigating disease-specific microbiome changes. This platform may support translational efforts to integrate microbiome insights into clinical research, therapeutic development, and personalized medicine. In conclusion, this novel bioreactor-based in vitro model, MyBioScope, shows strong potential for in-depth exploration of disease-specific microbiomes and can facilitate new ways for integrating the knowledge of the microbiome’s impact on human health and disease into clinical practice.
GRAPHICAL ABSTRACT: [Image: see text]
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s40643-026-01044-1.},
}
RevDate: 2026-05-23
Gut microbiome-mediated bioactive ingredients and health benefits of medicinal and edible fermented products: A comprehensive review.
Folia microbiologica [Epub ahead of print].
Fermented foods and beverages represent dynamic biological ecosystems that integrate microbial communities, bioactive metabolites, and host interactions to promote health across nutritional, functional, and therapeutic domains. This comprehensive narrative review synthesizes current evidence on medicinal and edible fermented products, focusing on their bioactive generation, molecular mechanisms, and systemic health outcomes mediated by the gut microbiome. Fermentation processes, driven by lactic acid bacteria, yeasts, and mixed consortia, transform substrates into 31 key bioactives, including short-chain fatty acids (SCFAs), bioactive peptides, exopolysaccharides (EPS), and modified polyphenols. These compounds arise through microbial proteolysis, glycolysis, and biotransformation, enhancing bioavailability and functionality compared to unfermented counterparts. Mechanistically, bioactives strengthen gut barrier integrity via tight-junction upregulation and mucin production; modulate immunity through Toll-like receptor activation and T-cell differentiation; regulate metabolism by improving glucose/lipid profiles; and mitigate inflammation via NF-κB inhibition and Nrf2 activation. Gut microbiota-host crosstalk extends these effects systemically, influencing the gut-brain axis and extra-intestinal organs. Epidemiological and clinical data link regular consumption particularly of yogurt, kimchi, and kefir-to reduced risks of colorectal cancer (dose-response patterns), type 2 diabetes (8-15% HbA1c reductions), cardiovascular disease (5-10% cholesterol lowering), and enhanced immune resilience (20-35% fewer infections). Benefits also encompass gastrointestinal health (IBS symptom relief), neuroprotection (cognitive improvements), and cancer prevention. Despite promising findings, challenges persist in standardization, microbial viability during processing, and long-term human trials. Future directions emphasize multi-omics integration, AI-driven precision fermentation, and personalized interventions to validate fermented products as evidence-based therapeutics, bridging traditional practices with modern nutrition science.
Additional Links: PMID-42176172
PubMed:
Citation:
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@article {pmid42176172,
year = {2026},
author = {Liu, C and Zhang, S and Yue, Q and Sun, X and Zheng, K and Li, K and Su, L and Zhao, L},
title = {Gut microbiome-mediated bioactive ingredients and health benefits of medicinal and edible fermented products: A comprehensive review.},
journal = {Folia microbiologica},
volume = {},
number = {},
pages = {},
pmid = {42176172},
issn = {1874-9356},
abstract = {Fermented foods and beverages represent dynamic biological ecosystems that integrate microbial communities, bioactive metabolites, and host interactions to promote health across nutritional, functional, and therapeutic domains. This comprehensive narrative review synthesizes current evidence on medicinal and edible fermented products, focusing on their bioactive generation, molecular mechanisms, and systemic health outcomes mediated by the gut microbiome. Fermentation processes, driven by lactic acid bacteria, yeasts, and mixed consortia, transform substrates into 31 key bioactives, including short-chain fatty acids (SCFAs), bioactive peptides, exopolysaccharides (EPS), and modified polyphenols. These compounds arise through microbial proteolysis, glycolysis, and biotransformation, enhancing bioavailability and functionality compared to unfermented counterparts. Mechanistically, bioactives strengthen gut barrier integrity via tight-junction upregulation and mucin production; modulate immunity through Toll-like receptor activation and T-cell differentiation; regulate metabolism by improving glucose/lipid profiles; and mitigate inflammation via NF-κB inhibition and Nrf2 activation. Gut microbiota-host crosstalk extends these effects systemically, influencing the gut-brain axis and extra-intestinal organs. Epidemiological and clinical data link regular consumption particularly of yogurt, kimchi, and kefir-to reduced risks of colorectal cancer (dose-response patterns), type 2 diabetes (8-15% HbA1c reductions), cardiovascular disease (5-10% cholesterol lowering), and enhanced immune resilience (20-35% fewer infections). Benefits also encompass gastrointestinal health (IBS symptom relief), neuroprotection (cognitive improvements), and cancer prevention. Despite promising findings, challenges persist in standardization, microbial viability during processing, and long-term human trials. Future directions emphasize multi-omics integration, AI-driven precision fermentation, and personalized interventions to validate fermented products as evidence-based therapeutics, bridging traditional practices with modern nutrition science.},
}
RevDate: 2026-05-23
Freeze-thaw specifically regulates microbiome patterns and phosphorus acquisition strategies in the lake-groundwater interaction zone.
Water research, 302:126129 pii:S0043-1354(26)00809-2 [Epub ahead of print].
Freeze-thaw regulates phosphorus cycling in lake-groundwater interaction zones (LIZ) of seasonally frozen regions, where microorganisms and their functional traits play indispensable roles. However, the spatiotemporal dynamics of phosphorus pools and their driving mechanisms in the LIZ remain poorly understood, especially with insufficient quantitative evidence. Using absolute quantitative metagenomics, this study investigated the LIZ of Lake Chagan, a typical eutrophic lake in the seasonally frozen region. Results showed that Losses of Fe-P (44.69%) and Res-P (35.47%) dominated sediment phosphorus dynamics. Freeze-thaw induced opposing trends in diversity and similarity of PCGs-microbial communities between sediment and the lake-groundwater. The assembly of PCGs-microbial communities shifted from stochastic to deterministic processes in lake-groundwater, while stochastic processes persisted in sediments. DIP and DOP in lake-groundwater were driven by genes involved in P-uptake and transport (r = 0.65 and 0.40, respectively, P<0.05), while phosphorus release from sediments was co-regulated by inorganic P-solubilization and organic P-mineralization genes (r = 0.89 and -0.36, respectively, P<0.05). Microbial taxa harboring complete phosphorus cycling pathways (42.2%) and organic P-mineralization genes (48.1%) were relatively rare, with Pseudomonadota as the dominant phylum (65.2% and 57.0%, respectively). This study reveals medium-specific adaptive strategies of microorganisms and PCGs-mediated phosphorus cycling mechanisms, providing scientific support for predicting eutrophication risks and managing lake ecosystems in seasonally frozen regions.
Additional Links: PMID-42176375
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PubMed:
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@article {pmid42176375,
year = {2026},
author = {Zhang, Y and Wang, R and Su, X and Lang, T and Li, D},
title = {Freeze-thaw specifically regulates microbiome patterns and phosphorus acquisition strategies in the lake-groundwater interaction zone.},
journal = {Water research},
volume = {302},
number = {},
pages = {126129},
doi = {10.1016/j.watres.2026.126129},
pmid = {42176375},
issn = {1879-2448},
abstract = {Freeze-thaw regulates phosphorus cycling in lake-groundwater interaction zones (LIZ) of seasonally frozen regions, where microorganisms and their functional traits play indispensable roles. However, the spatiotemporal dynamics of phosphorus pools and their driving mechanisms in the LIZ remain poorly understood, especially with insufficient quantitative evidence. Using absolute quantitative metagenomics, this study investigated the LIZ of Lake Chagan, a typical eutrophic lake in the seasonally frozen region. Results showed that Losses of Fe-P (44.69%) and Res-P (35.47%) dominated sediment phosphorus dynamics. Freeze-thaw induced opposing trends in diversity and similarity of PCGs-microbial communities between sediment and the lake-groundwater. The assembly of PCGs-microbial communities shifted from stochastic to deterministic processes in lake-groundwater, while stochastic processes persisted in sediments. DIP and DOP in lake-groundwater were driven by genes involved in P-uptake and transport (r = 0.65 and 0.40, respectively, P<0.05), while phosphorus release from sediments was co-regulated by inorganic P-solubilization and organic P-mineralization genes (r = 0.89 and -0.36, respectively, P<0.05). Microbial taxa harboring complete phosphorus cycling pathways (42.2%) and organic P-mineralization genes (48.1%) were relatively rare, with Pseudomonadota as the dominant phylum (65.2% and 57.0%, respectively). This study reveals medium-specific adaptive strategies of microorganisms and PCGs-mediated phosphorus cycling mechanisms, providing scientific support for predicting eutrophication risks and managing lake ecosystems in seasonally frozen regions.},
}
RevDate: 2026-05-23
Valorization of vitamin C industrial byproduct as a soil amendment: Environmental benefits and enhancement of maize productivity.
Journal of environmental management, 409:129982 pii:S0301-4797(26)01442-8 [Epub ahead of print].
The mechanisms by which vitamin C residue after evaporation (RAE) regulates soil microbial processes and maize productivity remain unclear. A randomized complete block field trial was conducted in 2023. The trial evaluated the effects of RAE on soil nutrient availability, microbial functional potential, and maize productivity, with three treatments: (1) untreated control (CK), (2) low RAE rate (LR: 150 L/ha), and (3) high RAE rate (HR: 300 L/ha), each with four replicates. RAE was applied through drip irrigation at the six-leaf and fourteen-leaf stages of maize. RAE application increased soil dissolved organic carbon (5.75-16.73%) and mineral nitrogen availability, with ammonium and nitrate increasing by 24.79-51.04% and 23.24-69.25%, respectively, whereas soil organic carbon and total nitrogen, phosphorus, and potassium were unchanged. RAE also increased soil microbial biomass, soil respiration, and key enzymes involved in carbon, nitrogen, and phosphorus cycling, whereas HR shifted bacterial community composition and increased copy numbers of functional genes involved in these processes. RAE further enhanced maize physiological performance: photosynthetic rate increased by 12.88-33.41%, relative chlorophyll content (SPAD) by 9.73-25.10%, and dry matter translocation by 18.79-31.93%, resulting in a grain yield increase of 8.26-13.46% in 2023. Grain yield was recorded during 2023-2025, confirming the stability of this yield response. RAE application enhanced soil nutrient availability and microbial functional potential, thereby improving maize physiological performance and grain yield, likely through the regulation of nutrient cycling and microbial processes. These findings provide a value-added management strategy for utilizing RAE in agroecosystems.
Additional Links: PMID-42176539
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@article {pmid42176539,
year = {2026},
author = {Cheng, H and Sun, H and Gu, J and Yang, W and Gao, M and Xu, H},
title = {Valorization of vitamin C industrial byproduct as a soil amendment: Environmental benefits and enhancement of maize productivity.},
journal = {Journal of environmental management},
volume = {409},
number = {},
pages = {129982},
doi = {10.1016/j.jenvman.2026.129982},
pmid = {42176539},
issn = {1095-8630},
abstract = {The mechanisms by which vitamin C residue after evaporation (RAE) regulates soil microbial processes and maize productivity remain unclear. A randomized complete block field trial was conducted in 2023. The trial evaluated the effects of RAE on soil nutrient availability, microbial functional potential, and maize productivity, with three treatments: (1) untreated control (CK), (2) low RAE rate (LR: 150 L/ha), and (3) high RAE rate (HR: 300 L/ha), each with four replicates. RAE was applied through drip irrigation at the six-leaf and fourteen-leaf stages of maize. RAE application increased soil dissolved organic carbon (5.75-16.73%) and mineral nitrogen availability, with ammonium and nitrate increasing by 24.79-51.04% and 23.24-69.25%, respectively, whereas soil organic carbon and total nitrogen, phosphorus, and potassium were unchanged. RAE also increased soil microbial biomass, soil respiration, and key enzymes involved in carbon, nitrogen, and phosphorus cycling, whereas HR shifted bacterial community composition and increased copy numbers of functional genes involved in these processes. RAE further enhanced maize physiological performance: photosynthetic rate increased by 12.88-33.41%, relative chlorophyll content (SPAD) by 9.73-25.10%, and dry matter translocation by 18.79-31.93%, resulting in a grain yield increase of 8.26-13.46% in 2023. Grain yield was recorded during 2023-2025, confirming the stability of this yield response. RAE application enhanced soil nutrient availability and microbial functional potential, thereby improving maize physiological performance and grain yield, likely through the regulation of nutrient cycling and microbial processes. These findings provide a value-added management strategy for utilizing RAE in agroecosystems.},
}
RevDate: 2026-05-23
Trichoderma modulates Pseudomonas metabolism: Co-inoculation enhances phosphorus acquisition of Pyrus betulifolia in calcareous soil.
Microbiological research, 310:128552 pii:S0944-5013(26)00116-3 [Epub ahead of print].
Phosphorus (P) is poorly available in calcareous soils, limiting pear growth. We evaluated whether Trichoderma brevicompactum TB2 improves P availability and the rhizosphere microbiome. This study used Trichoderma brevicompactum TB2 to investigate the regulatory mechanisms influencing rhizosphere phosphorus transformation and microbiome structure in pear seedlings. Four treatments were analyzed: sterilized soil control (SSC), sterilized soil with TB2 (SST), natural soil control (NSC), and natural soil with TB2 (NST). SST and NST treatments significantly increased plant height, biomass, and soil available phosphorus (AP) while reducing soil pH compared to SSC and NSC. Notably, only the NST treatment significantly enhanced plant phosphorus content and accumulation. Compared to NSC, NST led to significant restructuring of the rhizosphere microbial community (via 16S rRNA) and functional differentiation in phosphorus cycling (as shown by metagenomics), including increased abundances of key phosphorus-metabolism genes (phnN, phnL, phnP, gcd) and improved organic phosphoester hydrolysis and transport pathways. Metagenome-assembled genomes (MAGs) identified five high-quality gcd-containing MAGs, including those from Bacteroidota (bin43, bin16) and Pseudomonas (bin53, bin72, bin13), with a bin13-match strain isolated from the NST rhizosphere. Pot trials confirmed that inoculation with TB2 or PSE significantly improved plant biomass and phosphorus nutrition indices compared to CK. Co-inoculation with TB2 and PSE elicited synergistic effects that exceeded those of the individual inoculants. In natural calcareous soil, TB2 enhances pear growth by recruiting P-solubilizing Pseudomonas and activating rhizosphere P cycling. This offers a practical route to improve P-fertilizer efficiency in orchards.
Additional Links: PMID-42176589
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@article {pmid42176589,
year = {2026},
author = {Kuerban, Z and Shao, Y and Jiang, R and Shi, Y and Ma, Y and Li, H and Mei, X and Xu, Y and Dong, C and Shen, Q},
title = {Trichoderma modulates Pseudomonas metabolism: Co-inoculation enhances phosphorus acquisition of Pyrus betulifolia in calcareous soil.},
journal = {Microbiological research},
volume = {310},
number = {},
pages = {128552},
doi = {10.1016/j.micres.2026.128552},
pmid = {42176589},
issn = {1618-0623},
abstract = {Phosphorus (P) is poorly available in calcareous soils, limiting pear growth. We evaluated whether Trichoderma brevicompactum TB2 improves P availability and the rhizosphere microbiome. This study used Trichoderma brevicompactum TB2 to investigate the regulatory mechanisms influencing rhizosphere phosphorus transformation and microbiome structure in pear seedlings. Four treatments were analyzed: sterilized soil control (SSC), sterilized soil with TB2 (SST), natural soil control (NSC), and natural soil with TB2 (NST). SST and NST treatments significantly increased plant height, biomass, and soil available phosphorus (AP) while reducing soil pH compared to SSC and NSC. Notably, only the NST treatment significantly enhanced plant phosphorus content and accumulation. Compared to NSC, NST led to significant restructuring of the rhizosphere microbial community (via 16S rRNA) and functional differentiation in phosphorus cycling (as shown by metagenomics), including increased abundances of key phosphorus-metabolism genes (phnN, phnL, phnP, gcd) and improved organic phosphoester hydrolysis and transport pathways. Metagenome-assembled genomes (MAGs) identified five high-quality gcd-containing MAGs, including those from Bacteroidota (bin43, bin16) and Pseudomonas (bin53, bin72, bin13), with a bin13-match strain isolated from the NST rhizosphere. Pot trials confirmed that inoculation with TB2 or PSE significantly improved plant biomass and phosphorus nutrition indices compared to CK. Co-inoculation with TB2 and PSE elicited synergistic effects that exceeded those of the individual inoculants. In natural calcareous soil, TB2 enhances pear growth by recruiting P-solubilizing Pseudomonas and activating rhizosphere P cycling. This offers a practical route to improve P-fertilizer efficiency in orchards.},
}
RevDate: 2026-05-23
Cross-scale mechanisms and molecular-ecological thresholds of phthalate stress in the cucumber-soil system.
Journal of hazardous materials, 513:142398 pii:S0304-3894(26)01376-2 [Epub ahead of print].
Phthalates (PAEs) are widespread soil contaminants that threaten the sustainability of agricultural lands, yet the threshold mechanism by which they trigger collapse of the cucumber-soil system remains unclear. Integrating physiological, ultrastructural, proteomic, and microbiome analyses, this study tracked the dose-response of the cucumber-soil system to PAEs (0, 5, and 15 mg/kg). A biphasic response was identified: 5 mg/kg induced "reversible compensation," where upregulated antioxidant enzymes and proline preserved physiological function and high rhizosphere bacterial diversity. Conversely, 15 mg/kg triggered "irreversible collapse." Proteomics and pathway modeling revealed the core mechanism: despite a burst in GST synthesis, the failure of the ASA-GSH regeneration cycle caused a redox collapse (GSH/GSSG ≈ 0.02) and subsequent organelle disintegration. Concurrently, the rhizosphere microbiome underwent structural simplification, shifting from a complex cooperative network to one dominated by tolerant taxa (Bacillus, Sphingomonas). By identifying the topological flip from protective to destructive regulation, this study establishes a cross-scale "molecular-ecological" threshold framework, providing a quantifiable scientific basis for hierarchical risk management in PAEs-contaminated farmland.
Additional Links: PMID-42176620
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PubMed:
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@article {pmid42176620,
year = {2026},
author = {Li, Z and Wang, L and Tuo, D and Huang, F and Shi, Y and Zhang, Y},
title = {Cross-scale mechanisms and molecular-ecological thresholds of phthalate stress in the cucumber-soil system.},
journal = {Journal of hazardous materials},
volume = {513},
number = {},
pages = {142398},
doi = {10.1016/j.jhazmat.2026.142398},
pmid = {42176620},
issn = {1873-3336},
abstract = {Phthalates (PAEs) are widespread soil contaminants that threaten the sustainability of agricultural lands, yet the threshold mechanism by which they trigger collapse of the cucumber-soil system remains unclear. Integrating physiological, ultrastructural, proteomic, and microbiome analyses, this study tracked the dose-response of the cucumber-soil system to PAEs (0, 5, and 15 mg/kg). A biphasic response was identified: 5 mg/kg induced "reversible compensation," where upregulated antioxidant enzymes and proline preserved physiological function and high rhizosphere bacterial diversity. Conversely, 15 mg/kg triggered "irreversible collapse." Proteomics and pathway modeling revealed the core mechanism: despite a burst in GST synthesis, the failure of the ASA-GSH regeneration cycle caused a redox collapse (GSH/GSSG ≈ 0.02) and subsequent organelle disintegration. Concurrently, the rhizosphere microbiome underwent structural simplification, shifting from a complex cooperative network to one dominated by tolerant taxa (Bacillus, Sphingomonas). By identifying the topological flip from protective to destructive regulation, this study establishes a cross-scale "molecular-ecological" threshold framework, providing a quantifiable scientific basis for hierarchical risk management in PAEs-contaminated farmland.},
}
RevDate: 2026-05-23
Beyond Endoscopy, Toward Innovative Diagnosis and Monitoring of Eosinophilic Gastrointestinal Diseases.
The journal of allergy and clinical immunology. In practice pii:S2213-2198(26)00421-6 [Epub ahead of print].
Currently, esophagogastroduodenoscopy (EGD) with biopsy is essential to the diagnosis and management of eosinophilic gastrointestinal diseases (EGIDs) to visually evaluate the gastrointestinal mucosa, obtain mucosal biopsies and assess treatment response as symptoms do not necessarily correlate with histology. To assess mucosal inflammation after initiating or modifying treatment, multiple repeat EGDs are commonly needed and are burdensome due to post-procedure recovery, costs and impact on quality-of-life. For these reasons, there is increasing interest in novel less invasive modalities in the management of EGIDs, particularly eosinophilic esophagitis (EoE). Here in, we review innovative modalities that may be used in lieu of EGD for EoE including unsedated transnasal endoscopy, esophageal string test, and sponge based devices; innovative modalities complementary to endoscopy such as impedance planimetry; we discuss the role of pH impendence monitoring and radiologic imaging in EoE and explore the future of non-invasive modalities including biomarkers and the microbiome.
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@article {pmid42176735,
year = {2026},
author = {Nguyen, N and Ackerman, SJ and Shoda, T and Katzka, D},
title = {Beyond Endoscopy, Toward Innovative Diagnosis and Monitoring of Eosinophilic Gastrointestinal Diseases.},
journal = {The journal of allergy and clinical immunology. In practice},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jaip.2026.05.017},
pmid = {42176735},
issn = {2213-2201},
abstract = {Currently, esophagogastroduodenoscopy (EGD) with biopsy is essential to the diagnosis and management of eosinophilic gastrointestinal diseases (EGIDs) to visually evaluate the gastrointestinal mucosa, obtain mucosal biopsies and assess treatment response as symptoms do not necessarily correlate with histology. To assess mucosal inflammation after initiating or modifying treatment, multiple repeat EGDs are commonly needed and are burdensome due to post-procedure recovery, costs and impact on quality-of-life. For these reasons, there is increasing interest in novel less invasive modalities in the management of EGIDs, particularly eosinophilic esophagitis (EoE). Here in, we review innovative modalities that may be used in lieu of EGD for EoE including unsedated transnasal endoscopy, esophageal string test, and sponge based devices; innovative modalities complementary to endoscopy such as impedance planimetry; we discuss the role of pH impendence monitoring and radiologic imaging in EoE and explore the future of non-invasive modalities including biomarkers and the microbiome.},
}
RevDate: 2026-05-25
Neuronutrition in ASD: Involvement of gut microbiota, oxidative stress and inflammatory markers.
Neuroscience and biobehavioral reviews, 187:106775 pii:S0149-7634(26)00232-0 [Epub ahead of print].
Autism spectrum disorder (ASD) is a neurodevelopmental disorder displaying altered human behaviors, such as social interaction impairments, stereotypical/repetitive activities and emotional dysregulation. Children with ASD are often affected by gastrointestinal problems and gut microbiota dysbiosis. Inflammation and immune dysfunction are key contributors to ASD, as shown by high proinflammatory cytokines and oxidative stress. Indeed, notable implication of the nuclear factor kappa B in the severity of ASD derives from its ability to amplify neuroinflammation. This narrative review focused attention on neuronutrition and gut microbiota manipulation for mitigation of ASD symptoms, including neuroinflammation and oxidative stress. Studies in both rodents and humans with ASD have revealed that both pure and mixed Lactobacillus and Bifidobacterium were effective in ameliorating behavioral symptoms and GABA/glutamate imbalance. Often, the combined use of probiotics and prebiotics can have greater health benefits in ASD. Additionally, dietary interventions and microbiota transfer therapies along with low-to-moderate-intensity exercise have been proposed to improve gastrointestinal and behavioral symptoms. However, despite some encouraging results, biases in the neuronutrition/microbiota literature still exist. Indeed, many studies rely on small sample sizes, cross-sectional designs, and heterogeneous populations that differ in diet, medications, and comorbidities. In this context, the development of a precision diet tailored to individual gut microbiome profiles will allow for a broader understanding of the microbial ecosystem and relative therapeutical applications. Hence, by integrating metagenomics, metabolomics, epigenomics, with evaluation of environmental and nutritional factors, it will be possible to significantly improve the quality of life for people with ASD and their families.
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@article {pmid42176766,
year = {2026},
author = {Avolio, E and Olivito, I and Minervini, D and Soda, T and De Bartolo, A and Rocca, C and Alò, R and Facciolo, RM},
title = {Neuronutrition in ASD: Involvement of gut microbiota, oxidative stress and inflammatory markers.},
journal = {Neuroscience and biobehavioral reviews},
volume = {187},
number = {},
pages = {106775},
doi = {10.1016/j.neubiorev.2026.106775},
pmid = {42176766},
issn = {1873-7528},
abstract = {Autism spectrum disorder (ASD) is a neurodevelopmental disorder displaying altered human behaviors, such as social interaction impairments, stereotypical/repetitive activities and emotional dysregulation. Children with ASD are often affected by gastrointestinal problems and gut microbiota dysbiosis. Inflammation and immune dysfunction are key contributors to ASD, as shown by high proinflammatory cytokines and oxidative stress. Indeed, notable implication of the nuclear factor kappa B in the severity of ASD derives from its ability to amplify neuroinflammation. This narrative review focused attention on neuronutrition and gut microbiota manipulation for mitigation of ASD symptoms, including neuroinflammation and oxidative stress. Studies in both rodents and humans with ASD have revealed that both pure and mixed Lactobacillus and Bifidobacterium were effective in ameliorating behavioral symptoms and GABA/glutamate imbalance. Often, the combined use of probiotics and prebiotics can have greater health benefits in ASD. Additionally, dietary interventions and microbiota transfer therapies along with low-to-moderate-intensity exercise have been proposed to improve gastrointestinal and behavioral symptoms. However, despite some encouraging results, biases in the neuronutrition/microbiota literature still exist. Indeed, many studies rely on small sample sizes, cross-sectional designs, and heterogeneous populations that differ in diet, medications, and comorbidities. In this context, the development of a precision diet tailored to individual gut microbiome profiles will allow for a broader understanding of the microbial ecosystem and relative therapeutical applications. Hence, by integrating metagenomics, metabolomics, epigenomics, with evaluation of environmental and nutritional factors, it will be possible to significantly improve the quality of life for people with ASD and their families.},
}
RevDate: 2026-05-23
Therapeutic Efficacy and Antigenicity of a Novel PEGylated IgA Protease in Preclinical Models of IgA Nephropathy.
Kidney international pii:S0085-2538(26)00401-1 [Epub ahead of print].
INTRODUCTION: IgA nephropathy is the most common primary glomerulonephritis worldwide, characterized by IgA deposition and a high risk of progression to kidney failure. While emerging therapies target IgA production or downstream inflammation, strategies to directly clear established IgA deposits from the kidney remain underexplored. Here, we evaluate a novel therapeutic IgA protease for its ability to clear glomerular IgA deposits and restore normal histology.
METHODS: The recombinant IgA protease was derived from Thomasclavelia ramosa (strain AK183), a human commensal bacterium presumed to have evolved for mutual tolerance within the microbiome with the host. The enzyme was PEGylated to reduce immunogenicity and prolong its half-life, producing the drug product PEG-AK183. We characterized its ex vivo potency and pharmacokinetic-pharmacodynamic profile in mice, then assessed therapeutic efficacy over eight weeks.
RESULTS: In vitro, a single molecule of PEG-AK183 cleaved between 500 and 1000 hIgA1 molecules in 60 minutes, demonstrating high catalytic efficiency. A single injection into human IgA1 (hIgA1) transgenic mice induced complete clearance of serum hIgA1 for up to eight days. Following eight-week weekly treatments, PEG-AK183 reduced circulating IgA and immune complex levels by approximately 80% and completely cleared glomerular IgA and associated complement C3 deposits. This was accompanied by a 45.5% reduction in proteinuria and significant improvements in histopathological indices, including mesangial proliferation and endocapillary hypercellularity. No treatment-related adverse effects were observed, including abnormalities in intestinal plasma B cells, hepatotoxicity, or the anti-drug antibody development, supporting a favorable safety profile for long-term, repeated administration.
CONCLUSIONS: Our preclinical study demonstrated that the engineered IgA degrader PEGAK183 is a potent, effective, and safe therapeutic in a humanized IgA nephropathy mouse model. By achieving sustained clearance of pathogenic IgA from both circulation and glomerular deposits, this IgA-protease-based therapy represents a promising candidate for the future treatment of IgA nephropathy.
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@article {pmid42176777,
year = {2026},
author = {Shen, X and Shu, C and Dong, Y and Li, J and Li, R and Zan, J and Xie, X and Jin, J and Zhang, H and Lv, J},
title = {Therapeutic Efficacy and Antigenicity of a Novel PEGylated IgA Protease in Preclinical Models of IgA Nephropathy.},
journal = {Kidney international},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.kint.2026.04.020},
pmid = {42176777},
issn = {1523-1755},
abstract = {INTRODUCTION: IgA nephropathy is the most common primary glomerulonephritis worldwide, characterized by IgA deposition and a high risk of progression to kidney failure. While emerging therapies target IgA production or downstream inflammation, strategies to directly clear established IgA deposits from the kidney remain underexplored. Here, we evaluate a novel therapeutic IgA protease for its ability to clear glomerular IgA deposits and restore normal histology.
METHODS: The recombinant IgA protease was derived from Thomasclavelia ramosa (strain AK183), a human commensal bacterium presumed to have evolved for mutual tolerance within the microbiome with the host. The enzyme was PEGylated to reduce immunogenicity and prolong its half-life, producing the drug product PEG-AK183. We characterized its ex vivo potency and pharmacokinetic-pharmacodynamic profile in mice, then assessed therapeutic efficacy over eight weeks.
RESULTS: In vitro, a single molecule of PEG-AK183 cleaved between 500 and 1000 hIgA1 molecules in 60 minutes, demonstrating high catalytic efficiency. A single injection into human IgA1 (hIgA1) transgenic mice induced complete clearance of serum hIgA1 for up to eight days. Following eight-week weekly treatments, PEG-AK183 reduced circulating IgA and immune complex levels by approximately 80% and completely cleared glomerular IgA and associated complement C3 deposits. This was accompanied by a 45.5% reduction in proteinuria and significant improvements in histopathological indices, including mesangial proliferation and endocapillary hypercellularity. No treatment-related adverse effects were observed, including abnormalities in intestinal plasma B cells, hepatotoxicity, or the anti-drug antibody development, supporting a favorable safety profile for long-term, repeated administration.
CONCLUSIONS: Our preclinical study demonstrated that the engineered IgA degrader PEGAK183 is a potent, effective, and safe therapeutic in a humanized IgA nephropathy mouse model. By achieving sustained clearance of pathogenic IgA from both circulation and glomerular deposits, this IgA-protease-based therapy represents a promising candidate for the future treatment of IgA nephropathy.},
}
RevDate: 2026-05-23
Gut microbial differences and function in infants with gastroschisis: a pilot prospective cohort study.
Beneficial microbes [Epub ahead of print].
Newborns with gastroschisis hospitalised in the neonatal intensive care unit (NICU) are at risk for a disrupted gut microbiome. Infants with gastroschisis are particularly vulnerable to a dysbiotic microbiome; they require prolonged parenteral nutrition (PN) due to intestinal dysmotility, which often leads to growth faltering (GF). This pilot study's goals were to (1) compare the gut microbiome in infants with gastroschisis to infants admitted to the NICU without congenital anomalies, (2) identify differences in the gut microbiome between infants with gastroschisis requiring prolonged PN and those who do not, and (3) compare the microbiome in infants with gastroschisis with GF to those without GF. This was a multi-site prospective cohort study including 17 infants born with gastroschisis and 16 infants with a gestational age greater than 34 weeks admitted to the NICU without congenital anomalies (controls). Prolonged PN was defined as more than 28 days. GF was defined as a decline in weight or length z-score from birth to discharge of ≤-0.8. Stool samples were collected weekly during hospitalisation and analysed by shotgun metagenomics to assess bacterial composition, diversity, and function. Gestational age and birth weight were similar in the gastroschisis group and the control group. Infants with gastroschisis showed increased Staphylococcus aureus and decreased Bifidobacterium longum. Those requiring prolonged PN had a reduced abundance of genes in the glucosidase pathway compared to those who did not. Infants with GF showed a lower abundance of genes involved in the NAD-diphosphatase pathway compared to those without GF. Infants with gastroschisis display a distinct microbial composition and function compared to NICU infants without this condition. Among infants with gastroschisis, differences in bacterial functional capacity were observed in those who required prolonged PN and developed GF.
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@article {pmid42177038,
year = {2026},
author = {Strobel, KM and Leibel, SL and Bhute, S and Aja, E and Jacobs, JP and Calkins, K},
title = {Gut microbial differences and function in infants with gastroschisis: a pilot prospective cohort study.},
journal = {Beneficial microbes},
volume = {},
number = {},
pages = {1-14},
doi = {10.1163/18762891-bja00121},
pmid = {42177038},
issn = {1876-2891},
abstract = {Newborns with gastroschisis hospitalised in the neonatal intensive care unit (NICU) are at risk for a disrupted gut microbiome. Infants with gastroschisis are particularly vulnerable to a dysbiotic microbiome; they require prolonged parenteral nutrition (PN) due to intestinal dysmotility, which often leads to growth faltering (GF). This pilot study's goals were to (1) compare the gut microbiome in infants with gastroschisis to infants admitted to the NICU without congenital anomalies, (2) identify differences in the gut microbiome between infants with gastroschisis requiring prolonged PN and those who do not, and (3) compare the microbiome in infants with gastroschisis with GF to those without GF. This was a multi-site prospective cohort study including 17 infants born with gastroschisis and 16 infants with a gestational age greater than 34 weeks admitted to the NICU without congenital anomalies (controls). Prolonged PN was defined as more than 28 days. GF was defined as a decline in weight or length z-score from birth to discharge of ≤-0.8. Stool samples were collected weekly during hospitalisation and analysed by shotgun metagenomics to assess bacterial composition, diversity, and function. Gestational age and birth weight were similar in the gastroschisis group and the control group. Infants with gastroschisis showed increased Staphylococcus aureus and decreased Bifidobacterium longum. Those requiring prolonged PN had a reduced abundance of genes in the glucosidase pathway compared to those who did not. Infants with GF showed a lower abundance of genes involved in the NAD-diphosphatase pathway compared to those without GF. Infants with gastroschisis display a distinct microbial composition and function compared to NICU infants without this condition. Among infants with gastroschisis, differences in bacterial functional capacity were observed in those who required prolonged PN and developed GF.},
}
RevDate: 2026-05-23
CmpDate: 2026-05-23
Microbiome and microbial products as immunomodulators: Implications for gastrointestinal cancers.
Advances in protein chemistry and structural biology, 152:1-35.
The Hippocratic adage "all disease starts in the gut" remains pertinent as research uncovers how the gut microbiome and its products influence immunity and gastrointestinal cancers. The immune system's remarkable paradox lies in its ability to distinguish and tolerate trillions of beneficial microbes while defending against harmful pathogens to maintain health. Disruptions to this delicate balance, known as dysbiosis, contribute to chronic inflammation and create a favourable tumour development and progression environment. Microbial metabolites, such as- short-chain fatty acids and secondary bile acids further modulate inflammation, gut barrier integrity, and immune checkpoint pathways. Emerging microbial biomarkers show promise in diagnosis and prognosis and compete with traditional clinical factors. Innovative therapeutic strategies are being explored to harness the microbiome's immunomodulatory potential. Integrating microbiome profiling into personalised medicine offers new opportunities to prevent, detect, and treat gastrointestinal cancers, shifting the microbiome from a passive disease marker to an active agent that modulates and influences the disease. This chapter discusses the emerging understanding of microbiomes and microbial products in gastrointestinal cancers, highlighting diagnostic advances and novel therapeutic approaches that leverage microbial interactions to improve patient outcomes.
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@article {pmid42177066,
year = {2026},
author = {Yendreddy, SR and Patchigolla, D and Singh, S and Baghel, K and Ojha, R and Prajapati, VK},
title = {Microbiome and microbial products as immunomodulators: Implications for gastrointestinal cancers.},
journal = {Advances in protein chemistry and structural biology},
volume = {152},
number = {},
pages = {1-35},
doi = {10.1016/bs.apcsb.2025.10.008},
pmid = {42177066},
issn = {1876-1631},
mesh = {Humans ; *Gastrointestinal Neoplasms/immunology/microbiology/therapy/diagnosis ; *Gastrointestinal Microbiome/immunology ; },
abstract = {The Hippocratic adage "all disease starts in the gut" remains pertinent as research uncovers how the gut microbiome and its products influence immunity and gastrointestinal cancers. The immune system's remarkable paradox lies in its ability to distinguish and tolerate trillions of beneficial microbes while defending against harmful pathogens to maintain health. Disruptions to this delicate balance, known as dysbiosis, contribute to chronic inflammation and create a favourable tumour development and progression environment. Microbial metabolites, such as- short-chain fatty acids and secondary bile acids further modulate inflammation, gut barrier integrity, and immune checkpoint pathways. Emerging microbial biomarkers show promise in diagnosis and prognosis and compete with traditional clinical factors. Innovative therapeutic strategies are being explored to harness the microbiome's immunomodulatory potential. Integrating microbiome profiling into personalised medicine offers new opportunities to prevent, detect, and treat gastrointestinal cancers, shifting the microbiome from a passive disease marker to an active agent that modulates and influences the disease. This chapter discusses the emerging understanding of microbiomes and microbial products in gastrointestinal cancers, highlighting diagnostic advances and novel therapeutic approaches that leverage microbial interactions to improve patient outcomes.},
}
MeSH Terms:
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Humans
*Gastrointestinal Neoplasms/immunology/microbiology/therapy/diagnosis
*Gastrointestinal Microbiome/immunology
RevDate: 2026-05-23
Association of gut microbiome with mobility impairment in the Hispanic Community Health Study/Study of Latinos.
NPJ biofilms and microbiomes pii:10.1038/s41522-026-01019-2 [Epub ahead of print].
Aging-related declines in mobility are more common in women than men. The gut microbiome may play a role in physical function, but sex-specific roles are unknown. In adults ≥50 years old (n = 1187 women, 585 men), we examined associations of self-reported mobility impairment with gut microbiome assessed by stool shotgun sequencing, and examined heterogeneity by sex. Gut microbiome α-diversity was lower and overall composition (β-diversity) altered in women with mobility impairment compared to without, but this was not the case in men. Fifteen microbiome species were associated with mobility impairment in both women and men, including enrichment of Streptococcus and Lactobacillus and depletion of Eubacterium species. An additional 84 species were associated with mobility impairment in women only, including enrichment of Gammaproteobacteria species, but none were associated with mobility impairment in men only. Correlations of impaired mobility-related microbiome scores, derived from universal and women-specific microbiome species, with serum metabolites (n = 385) suggested that impaired mobility-related species may be involved in synthesis of imidazole propionate and deoxycholic acid metabolites, while species depleted with mobility impairment may be involved in sex hormone metabolism and guanidinoacetate production, the latter in women only. Gut microbiota may play a role in physical function and sex differences therein.
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@article {pmid42177172,
year = {2026},
author = {Peters, BA and Qi, Q and Xue, X and Moon, JY and Yu, B and Thomas, SN and Cordero, C and Daviglus, ML and Burk, RD and Kaplan, RC and Isasi, CR},
title = {Association of gut microbiome with mobility impairment in the Hispanic Community Health Study/Study of Latinos.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-01019-2},
pmid = {42177172},
issn = {2055-5008},
support = {R03HL182350/HL/NHLBI NIH HHS/United States ; R01DK134672/DK/NIDDK NIH HHS/United States ; R01AG085320/AG/NIA NIH HHS/United States ; },
abstract = {Aging-related declines in mobility are more common in women than men. The gut microbiome may play a role in physical function, but sex-specific roles are unknown. In adults ≥50 years old (n = 1187 women, 585 men), we examined associations of self-reported mobility impairment with gut microbiome assessed by stool shotgun sequencing, and examined heterogeneity by sex. Gut microbiome α-diversity was lower and overall composition (β-diversity) altered in women with mobility impairment compared to without, but this was not the case in men. Fifteen microbiome species were associated with mobility impairment in both women and men, including enrichment of Streptococcus and Lactobacillus and depletion of Eubacterium species. An additional 84 species were associated with mobility impairment in women only, including enrichment of Gammaproteobacteria species, but none were associated with mobility impairment in men only. Correlations of impaired mobility-related microbiome scores, derived from universal and women-specific microbiome species, with serum metabolites (n = 385) suggested that impaired mobility-related species may be involved in synthesis of imidazole propionate and deoxycholic acid metabolites, while species depleted with mobility impairment may be involved in sex hormone metabolism and guanidinoacetate production, the latter in women only. Gut microbiota may play a role in physical function and sex differences therein.},
}
RevDate: 2026-05-23
Preserving the gut microbiome: hydrogel-forming microneedle delivery of tetracycline reduces gut microbiome disruption compared to oral administration.
Drug delivery and translational research [Epub ahead of print].
Antibiotics cause significant gut microbiome dysbiosis, particularly when administered orally. This contributes to antimicrobial resistance (AMR) and is associated with myriad health conditions. Novel drug delivery strategies that minimize gut exposure while maintaining therapeutic efficacy are urgently needed. This study aimed to evaluate whether a novel transdermal system could reduce gut microbiome disruption compared to oral delivery. Sprague-Dawley rats received a single tetracycline dose via oral gavage, IV injection, or hydrogel-forming microneedle patch. Faecal samples were collected longitudinally and analysed using 16 S rRNA gene sequencing. Oral tetracycline caused the greatest disruption to gut microbiota. Compared to the timepoint immediately prior to treatment (Day 5a), peak dysbiosis was observed at Day 7. The Firmicutes: Bacteroidetes ratio was significantly reduced following oral and IV tetracycline therapy, but not following microneedle administration. The most significant reductions in alpha and beta diversity at Day 7 were observed in the oral group. Differential abundance analysis showed oral treatment resulted in the highest number of depleted and enriched taxa. The microbiome-sparing effect of microneedle delivery was consistent across all analytical measures, offering a promising strategy to preserve host microbiome health. This minimally invasive approach represents a clinically viable alternative to oral and IV antibiotic administration.
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@article {pmid42177348,
year = {2026},
author = {Kelly, SA and Zhao, L and Nzakizwanayo, J and Rodgers, AM and Thompson, TP and Lee, AJ and McCarthy, HO and McGrath, JW and Ingram, RJ and Jones, BV and Gilmore, BF and Donnelly, RF},
title = {Preserving the gut microbiome: hydrogel-forming microneedle delivery of tetracycline reduces gut microbiome disruption compared to oral administration.},
journal = {Drug delivery and translational research},
volume = {},
number = {},
pages = {},
pmid = {42177348},
issn = {2190-3948},
support = {UNS39792/WT_/Wellcome Trust/United Kingdom ; },
abstract = {Antibiotics cause significant gut microbiome dysbiosis, particularly when administered orally. This contributes to antimicrobial resistance (AMR) and is associated with myriad health conditions. Novel drug delivery strategies that minimize gut exposure while maintaining therapeutic efficacy are urgently needed. This study aimed to evaluate whether a novel transdermal system could reduce gut microbiome disruption compared to oral delivery. Sprague-Dawley rats received a single tetracycline dose via oral gavage, IV injection, or hydrogel-forming microneedle patch. Faecal samples were collected longitudinally and analysed using 16 S rRNA gene sequencing. Oral tetracycline caused the greatest disruption to gut microbiota. Compared to the timepoint immediately prior to treatment (Day 5a), peak dysbiosis was observed at Day 7. The Firmicutes: Bacteroidetes ratio was significantly reduced following oral and IV tetracycline therapy, but not following microneedle administration. The most significant reductions in alpha and beta diversity at Day 7 were observed in the oral group. Differential abundance analysis showed oral treatment resulted in the highest number of depleted and enriched taxa. The microbiome-sparing effect of microneedle delivery was consistent across all analytical measures, offering a promising strategy to preserve host microbiome health. This minimally invasive approach represents a clinically viable alternative to oral and IV antibiotic administration.},
}
RevDate: 2026-05-23
A randomised clinical trial testing the safety of and metabolic responses to short-term duodenal infusion of recombinant RORDEP1 in healthy men.
Diabetologia [Epub ahead of print].
AIMS/HYPOTHESIS: RUMTOR-derived peptides (RORDEPs) 1 and 2 are polypeptides synthesised by specific strains of the human gut commensal Ruminococcus torques. Preclinical studies have shown that RORDEPs lower blood glucose via an impact on plasma incretins and an improvement of hepatic insulin sensitivity. In a randomised, placebo-controlled, crossover trial, we here explore the safety and tolerability of, as well as any metabolic responses to, a duodenal infusion of recombinant RORDEP1 (r-RORDEP1) given to healthy men after oral intake of a liquid mixed meal.
METHODS: Seventeen healthy, normal-weight men between 18 and 35 years of age were randomised through block randomisation to receive either r-RORDEP1 or placebo as the initial intervention at Gentofte Hospital, Denmark. Exclusion criteria were use of any form of medication, use of antibiotics during the 3 months before intervention, lactose intolerance, smoking, alcohol or drug abuse, or the use of probiotics or creatine as dietary supplements during the study period. Blocks were created prior to trial initiation. Both participants and investigators were blinded to treatment. Following intake of a standardised liquid meal, r-RORDEP1 was given via a naso-duodenal tube as an initial bolus of 0.0108 mg/kg body weight followed by a continuous infusion of 0.25 µg kg[-1] min[-1] for 170 min. Primary outcomes were changes in plasma concentrations of incretins and peptide YY, while secondary endpoints were safety and tolerability, and changes in plasma insulin, C-peptide and glucose.
RESULTS: All 17 participants completed the trial. Duodenal infusion of r-RORDEP1 was well tolerated and without changes in biochemical measures of haematological, liver or renal functions. Compared with placebo, the bolus of r-RORDEP1 induced an early (at 15 or 30 min) rise in plasma glucagon-like peptide-1, insulin and C-peptide (q=0.001, q=0.001 and q=0.003, respectively) and a decline in plasma gastric inhibitory polypeptide and glucose (q=0.02 and q=0.006, respectively), while also increasing whole-body insulin sensitivity as measured with the Matsuda index of insulin sensitivity (p=0.049).
CONCLUSIONS/INTERPRETATION: Short-term duodenal infusion of r-RORDEP1 is safe and well tolerated and elicits changes in plasma incretins, insulin and glucose, and a measure of whole-body insulin sensitivity, aligning with findings in rodents, supporting the hypothesis that RORDEPs hold a role in impacting host metabolism.
TRIAL REGISTRATION: ClinicalTrials.gov NCT06923839 FUNDING: EFSD/Lilly European Diabetes Research Programme 2021, RUCILP F-19235-01-64 - NNF21SA0070428 grant and NNF23SA0084103 grant, the latter two from the Novo Nordisk Foundation.
Additional Links: PMID-42177350
PubMed:
Citation:
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@article {pmid42177350,
year = {2026},
author = {Gæde, J and Fan, Y and Lyu, L and Gasbjerg, LS and Rossing, P and Hartmann, B and Holst, JJ and Lund, AB and Knop, FK and Pedersen, O},
title = {A randomised clinical trial testing the safety of and metabolic responses to short-term duodenal infusion of recombinant RORDEP1 in healthy men.},
journal = {Diabetologia},
volume = {},
number = {},
pages = {},
pmid = {42177350},
issn = {1432-0428},
support = {NNF21SA0070428//Novo Nordisk Fonden/ ; NNF23SA0084103//Novo Nordisk Fonden/ ; },
abstract = {AIMS/HYPOTHESIS: RUMTOR-derived peptides (RORDEPs) 1 and 2 are polypeptides synthesised by specific strains of the human gut commensal Ruminococcus torques. Preclinical studies have shown that RORDEPs lower blood glucose via an impact on plasma incretins and an improvement of hepatic insulin sensitivity. In a randomised, placebo-controlled, crossover trial, we here explore the safety and tolerability of, as well as any metabolic responses to, a duodenal infusion of recombinant RORDEP1 (r-RORDEP1) given to healthy men after oral intake of a liquid mixed meal.
METHODS: Seventeen healthy, normal-weight men between 18 and 35 years of age were randomised through block randomisation to receive either r-RORDEP1 or placebo as the initial intervention at Gentofte Hospital, Denmark. Exclusion criteria were use of any form of medication, use of antibiotics during the 3 months before intervention, lactose intolerance, smoking, alcohol or drug abuse, or the use of probiotics or creatine as dietary supplements during the study period. Blocks were created prior to trial initiation. Both participants and investigators were blinded to treatment. Following intake of a standardised liquid meal, r-RORDEP1 was given via a naso-duodenal tube as an initial bolus of 0.0108 mg/kg body weight followed by a continuous infusion of 0.25 µg kg[-1] min[-1] for 170 min. Primary outcomes were changes in plasma concentrations of incretins and peptide YY, while secondary endpoints were safety and tolerability, and changes in plasma insulin, C-peptide and glucose.
RESULTS: All 17 participants completed the trial. Duodenal infusion of r-RORDEP1 was well tolerated and without changes in biochemical measures of haematological, liver or renal functions. Compared with placebo, the bolus of r-RORDEP1 induced an early (at 15 or 30 min) rise in plasma glucagon-like peptide-1, insulin and C-peptide (q=0.001, q=0.001 and q=0.003, respectively) and a decline in plasma gastric inhibitory polypeptide and glucose (q=0.02 and q=0.006, respectively), while also increasing whole-body insulin sensitivity as measured with the Matsuda index of insulin sensitivity (p=0.049).
CONCLUSIONS/INTERPRETATION: Short-term duodenal infusion of r-RORDEP1 is safe and well tolerated and elicits changes in plasma incretins, insulin and glucose, and a measure of whole-body insulin sensitivity, aligning with findings in rodents, supporting the hypothesis that RORDEPs hold a role in impacting host metabolism.
TRIAL REGISTRATION: ClinicalTrials.gov NCT06923839 FUNDING: EFSD/Lilly European Diabetes Research Programme 2021, RUCILP F-19235-01-64 - NNF21SA0070428 grant and NNF23SA0084103 grant, the latter two from the Novo Nordisk Foundation.},
}
RevDate: 2026-05-23
SCRUM-Japan MONSTAR3 hematology cohort: a nationwide multi-omics integrated platform for next-generation precision medicine in hematologic malignancies.
International journal of clinical oncology [Epub ahead of print].
BACKGROUND: Hematologic malignancies exhibit marked biological heterogeneity that is often insufficiently characterized by genomic profiling alone. Integrated multi-omics approaches are required to enable more accurate prognostic stratification, elucidate resistance mechanisms, and identify therapeutic vulnerabilities across lymphoma, leukemia, and plasma cell neoplasms.
METHODS: SCRUM-Japan MONSTAR3 is a nationwide, prospective, integrated multi-omics platform. The hematology cohort aims to enroll 400 patients with newly diagnosed or relapsed/refractory hematologic malignancies. Tumor specimens-including bone marrow aspirates/biopsies or lymph node tissues-are collected at diagnosis and at relapse. The multi-omics workflow encompasses whole-exome sequencing, whole-transcriptome sequencing, spatial transcriptomics, plasma proteomics, metabolomics, microbiome analysis, and tumor-informed measurable residual disease (MRD) monitoring. MRD is assessed using next-generation sequencing-based immunoglobulin heavy (IgH) and T-cell receptor (TCR) rearrangement analysis for lymphoid malignancies and whole-genome sequencing-based variant tracking for myeloid malignancies.
RESULTS: Patient enrollment began in December 2024, followed by nationwide multicenter activation in November 2025. Multi-omics analyses have been implemented in a stepwise manner. Early operational indicators, including biospecimen acquisition, data quality control, and initiation of molecular assays, demonstrate the feasibility of coordinated nationwide deployment of this complex platform.
CONCLUSION: The MONSTAR3 hematology cohort represents the first nationwide integrated multi-omics initiative dedicated to hematologic malignancies. Its large scale, standardized biospecimen framework, and capacity to incorporate emerging technologies provide a robust infrastructure for molecular stratification, longitudinal disease monitoring, and hypothesis-driven interventional research, thereby advancing clinically actionable precision hematology.
Additional Links: PMID-42177352
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Citation:
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@article {pmid42177352,
year = {2026},
author = {Matsuda, K and Yuda, J and Yoshimaru, R and Harima, I and Sakuma, H and Uehara, A and Oto, M and Fukatsu, M and Ikezoe, T and Araie, H and Hosono, N and Ohwada, C and Nakaseko, C and Kakiuchi, S and Fujisawa, T and Hashimoto, T and Shibuki, T and Imai, M and Nagamine, M and Sakashita, S and Yamashita, R and Dodo, A and Horasawa, S and Nakamura, Y and Bando, H and Yoshino, T},
title = {SCRUM-Japan MONSTAR3 hematology cohort: a nationwide multi-omics integrated platform for next-generation precision medicine in hematologic malignancies.},
journal = {International journal of clinical oncology},
volume = {},
number = {},
pages = {},
pmid = {42177352},
issn = {1437-7772},
abstract = {BACKGROUND: Hematologic malignancies exhibit marked biological heterogeneity that is often insufficiently characterized by genomic profiling alone. Integrated multi-omics approaches are required to enable more accurate prognostic stratification, elucidate resistance mechanisms, and identify therapeutic vulnerabilities across lymphoma, leukemia, and plasma cell neoplasms.
METHODS: SCRUM-Japan MONSTAR3 is a nationwide, prospective, integrated multi-omics platform. The hematology cohort aims to enroll 400 patients with newly diagnosed or relapsed/refractory hematologic malignancies. Tumor specimens-including bone marrow aspirates/biopsies or lymph node tissues-are collected at diagnosis and at relapse. The multi-omics workflow encompasses whole-exome sequencing, whole-transcriptome sequencing, spatial transcriptomics, plasma proteomics, metabolomics, microbiome analysis, and tumor-informed measurable residual disease (MRD) monitoring. MRD is assessed using next-generation sequencing-based immunoglobulin heavy (IgH) and T-cell receptor (TCR) rearrangement analysis for lymphoid malignancies and whole-genome sequencing-based variant tracking for myeloid malignancies.
RESULTS: Patient enrollment began in December 2024, followed by nationwide multicenter activation in November 2025. Multi-omics analyses have been implemented in a stepwise manner. Early operational indicators, including biospecimen acquisition, data quality control, and initiation of molecular assays, demonstrate the feasibility of coordinated nationwide deployment of this complex platform.
CONCLUSION: The MONSTAR3 hematology cohort represents the first nationwide integrated multi-omics initiative dedicated to hematologic malignancies. Its large scale, standardized biospecimen framework, and capacity to incorporate emerging technologies provide a robust infrastructure for molecular stratification, longitudinal disease monitoring, and hypothesis-driven interventional research, thereby advancing clinically actionable precision hematology.},
}
RevDate: 2026-05-23
CmpDate: 2026-05-23
Scorpion gut microbiomes as a source of bioactive and rare actinobacteria with nonribosomal peptide potential.
Antonie van Leeuwenhoek, 119(6):.
Actinobacteria are well-known for their ability to produce bioactive secondary metabolites, including nonribosomal peptides (NRPs); however, many host-associated reservoirs remain underexplored. In this study, cultivable actinobacteria were isolated from scorpion gut, including both the intestinal tissue and its luminal contents, and evaluated their antimicrobial activity and presence of NRPs genes. Fifty scorpions (Odontobuthus doriae and Mesobuthus eupeus) were collected from Qom Province, Iran. Dissected gut homogenates were plated on selective media, yielding 120 pure isolates. Taxonomic identification was performed by 16S rRNA gene sequencing, antimicrobial activity was assessed using agar diffusion assays against a broad panel of bacteria and fungi, and isolates were screened for NRPS gene biosynthetic markers by PCR (using A3F/A7R primers). The collection was dominated by Streptomyces, with additional recovery of rarer genera such as Amycolatopsis and Nonomuraea. Overall, 57% of the isolates inhibited at least one test microorganisms, and some strains exhibited specific bioactivity, making them candidates for further investigation. NRPS amplicons (~ 700 bp) were detected in 33.3% of the isolates and were enriched among the 42.6% of bioactive isolates, suggesting a partial association between antimicrobial phenotypes and putative NRP biosynthetic capacity. Five isolates showed < 98.5% 16S rRNA similarity to described species, indicating potential taxonomic novelty. Collectively, these findings support scorpion guts as promising, niche-derived sources of diverse actinobacteria with antimicrobial activity and biosynthetic potential for natural product discovery.
Additional Links: PMID-42177354
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@article {pmid42177354,
year = {2026},
author = {Hashemian, N and Hamedi, J and Haghighat, S},
title = {Scorpion gut microbiomes as a source of bioactive and rare actinobacteria with nonribosomal peptide potential.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {6},
pages = {},
pmid = {42177354},
issn = {1572-9699},
mesh = {*Actinobacteria/genetics/isolation & purification/classification/metabolism ; *Scorpions/microbiology ; Animals ; *Gastrointestinal Microbiome ; RNA, Ribosomal, 16S/genetics ; Phylogeny ; DNA, Bacterial/genetics/chemistry ; Iran ; *Peptide Biosynthesis, Nucleic Acid-Independent ; *Peptides/metabolism ; },
abstract = {Actinobacteria are well-known for their ability to produce bioactive secondary metabolites, including nonribosomal peptides (NRPs); however, many host-associated reservoirs remain underexplored. In this study, cultivable actinobacteria were isolated from scorpion gut, including both the intestinal tissue and its luminal contents, and evaluated their antimicrobial activity and presence of NRPs genes. Fifty scorpions (Odontobuthus doriae and Mesobuthus eupeus) were collected from Qom Province, Iran. Dissected gut homogenates were plated on selective media, yielding 120 pure isolates. Taxonomic identification was performed by 16S rRNA gene sequencing, antimicrobial activity was assessed using agar diffusion assays against a broad panel of bacteria and fungi, and isolates were screened for NRPS gene biosynthetic markers by PCR (using A3F/A7R primers). The collection was dominated by Streptomyces, with additional recovery of rarer genera such as Amycolatopsis and Nonomuraea. Overall, 57% of the isolates inhibited at least one test microorganisms, and some strains exhibited specific bioactivity, making them candidates for further investigation. NRPS amplicons (~ 700 bp) were detected in 33.3% of the isolates and were enriched among the 42.6% of bioactive isolates, suggesting a partial association between antimicrobial phenotypes and putative NRP biosynthetic capacity. Five isolates showed < 98.5% 16S rRNA similarity to described species, indicating potential taxonomic novelty. Collectively, these findings support scorpion guts as promising, niche-derived sources of diverse actinobacteria with antimicrobial activity and biosynthetic potential for natural product discovery.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Actinobacteria/genetics/isolation & purification/classification/metabolism
*Scorpions/microbiology
Animals
*Gastrointestinal Microbiome
RNA, Ribosomal, 16S/genetics
Phylogeny
DNA, Bacterial/genetics/chemistry
Iran
*Peptide Biosynthesis, Nucleic Acid-Independent
*Peptides/metabolism
RevDate: 2026-05-23
The effects of parity on the maternal microbiome - challenges associated with mouse models.
Animal microbiome pii:10.1186/s42523-026-00582-5 [Epub ahead of print].
Understanding how parity shapes the maternal microbiota is critical for advancing maternal and offspring health. We investigated the effects of parity and spacing between births on the maternal microbiota in mice. While maternal age strongly influenced microbiota diversity and composition, parity and lengths of gaps between births showed minimal impact. These findings highlight key model constraints that must be considered when designing longitudinal microbiome studies within and beyond the context of reproduction.
Additional Links: PMID-42177592
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@article {pmid42177592,
year = {2026},
author = {Turjeman, S and Zgairy, S and Koren, O},
title = {The effects of parity on the maternal microbiome - challenges associated with mouse models.},
journal = {Animal microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s42523-026-00582-5},
pmid = {42177592},
issn = {2524-4671},
abstract = {Understanding how parity shapes the maternal microbiota is critical for advancing maternal and offspring health. We investigated the effects of parity and spacing between births on the maternal microbiota in mice. While maternal age strongly influenced microbiota diversity and composition, parity and lengths of gaps between births showed minimal impact. These findings highlight key model constraints that must be considered when designing longitudinal microbiome studies within and beyond the context of reproduction.},
}
RevDate: 2026-05-23
CmpDate: 2026-05-24
[1]H NMR-based metabolomics reveals metabolic changes in porcine ingesta and serum during Ascaris suum infection.
Parasites & vectors, 19(1):.
BACKGROUND: Roundworm infections are of major importance both for humans and livestock. The porcine roundworm Ascaris suum, the most economically important nematode in pig production worldwide, serves as a valuable model for human ascariosis, yet knowledge of its metabolic impact remains limited.
METHODS: Metabolic changes were investigated in pigs infected once with 10,000 A. suum eggs versus trickle-infected pigs (1000 eggs/day over 10 days) compared with uninfected controls. Ingesta and serum samples of six pigs each were collected on days 21, 35, and 49 post infection (pi) for nuclear magnetic resonance (NMR)-based metabolomics analyses.
RESULTS: Trickle-infected pigs showed more pronounced metabolic changes than single-infected pigs, following a triphasic temporal pattern with initial changes at day 21 pi, maximal disruption at day 35 pi, and partial recovery by day 49 pi. The colon exhibited the most significant changes in short-chain fatty acids (SCFAs) and amino acids. On day 21 pi, trickle-infected pigs showed increased acetate, butyrate, valerate, and amino acids in the colon, with reversed patterns on day 35 pi. Serum changes mirrored colonic alterations, suggesting the colon as primary driver of systemic responses. Single-infected pigs showed less pronounced changes, with increased lactate and acetate in the ileum and elevated amino acids in the cecum on day 35 pi.
CONCLUSIONS: These findings reveal complex, compartment-specific host-parasite-microbiome interactions, with SCFAs as important mediators. Enhanced growth performance in trickle-infected pigs corresponding with metabolic recovery challenges exclusively antagonistic host-parasite relationships. This study deepens the understanding of A. suum pathophysiology and provides crucial insights for human ascariosis, supporting targeted interventions for animal and human health.
Additional Links: PMID-42177600
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Citation:
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@article {pmid42177600,
year = {2026},
author = {Wagner, L and Springer, A and Koehler, S and Brüggemann, DA and Strube, C},
title = {[1]H NMR-based metabolomics reveals metabolic changes in porcine ingesta and serum during Ascaris suum infection.},
journal = {Parasites & vectors},
volume = {19},
number = {1},
pages = {},
pmid = {42177600},
issn = {1756-3305},
support = {STR 1171/16-1//Deutsche Forschungsgemeinschaft/ ; },
mesh = {Animals ; *Ascariasis/veterinary/parasitology/metabolism/blood ; *Ascaris suum/physiology ; Swine ; *Metabolomics ; *Swine Diseases/parasitology/metabolism/blood ; *Serum/chemistry ; Magnetic Resonance Spectroscopy ; Proton Magnetic Resonance Spectroscopy ; Colon/metabolism/parasitology ; Amino Acids/metabolism ; Fatty Acids, Volatile/metabolism ; Metabolome ; },
abstract = {BACKGROUND: Roundworm infections are of major importance both for humans and livestock. The porcine roundworm Ascaris suum, the most economically important nematode in pig production worldwide, serves as a valuable model for human ascariosis, yet knowledge of its metabolic impact remains limited.
METHODS: Metabolic changes were investigated in pigs infected once with 10,000 A. suum eggs versus trickle-infected pigs (1000 eggs/day over 10 days) compared with uninfected controls. Ingesta and serum samples of six pigs each were collected on days 21, 35, and 49 post infection (pi) for nuclear magnetic resonance (NMR)-based metabolomics analyses.
RESULTS: Trickle-infected pigs showed more pronounced metabolic changes than single-infected pigs, following a triphasic temporal pattern with initial changes at day 21 pi, maximal disruption at day 35 pi, and partial recovery by day 49 pi. The colon exhibited the most significant changes in short-chain fatty acids (SCFAs) and amino acids. On day 21 pi, trickle-infected pigs showed increased acetate, butyrate, valerate, and amino acids in the colon, with reversed patterns on day 35 pi. Serum changes mirrored colonic alterations, suggesting the colon as primary driver of systemic responses. Single-infected pigs showed less pronounced changes, with increased lactate and acetate in the ileum and elevated amino acids in the cecum on day 35 pi.
CONCLUSIONS: These findings reveal complex, compartment-specific host-parasite-microbiome interactions, with SCFAs as important mediators. Enhanced growth performance in trickle-infected pigs corresponding with metabolic recovery challenges exclusively antagonistic host-parasite relationships. This study deepens the understanding of A. suum pathophysiology and provides crucial insights for human ascariosis, supporting targeted interventions for animal and human health.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Ascariasis/veterinary/parasitology/metabolism/blood
*Ascaris suum/physiology
Swine
*Metabolomics
*Swine Diseases/parasitology/metabolism/blood
*Serum/chemistry
Magnetic Resonance Spectroscopy
Proton Magnetic Resonance Spectroscopy
Colon/metabolism/parasitology
Amino Acids/metabolism
Fatty Acids, Volatile/metabolism
Metabolome
RevDate: 2026-05-24
Exploratory gut microbiota-host interaction in parkinson's disease: integrative multi-omics analysis of metabolic and epigenetic pathways.
AMB Express pii:10.1186/s13568-026-02078-6 [Epub ahead of print].
Mounting evidence has associated gut microbial composition and systemic metabolic profiles with Parkinson's disease (PD), yet causal pathways and molecular mechanisms remain unclear. We employed a systematic two-stage analytical framework integrating multiple Mendelian randomization (MR) approaches, transcriptome and epigenome-wide regulatory analyses, and colocalization analysis to genetically dissect the microbiota-host regulatory network implicated in PD susceptibility. Initially, two-sample MR was performed using gut microbiota data from the MiBioGen consortium, followed by an independent replication MR analysis using mbQTL data from the Dutch Microbiome Project (DMP). The two-step MR approach was employed to identify potential mediation of blood metabolites. Summary data-based MR (SMR) methods were also used to pinpoint key blood metabolic genes and regulatory regions associated with PD risk, with the combination of PD GWAS data, blood expression quantitative trait loci (eQTLs), and DNA methylation quantitative trait loci (mQTLs). Colocalization analyses were performed to explore interactions between host metabolic gene expression and the gut microbiota using blood expression quantitative trait loci (eQTLs) and fecal microbial quantitative trait loci (mbQTLs). Our multi-stage analyses identified five microbial taxa with nominal positive associations with Parkinson's disease (PD), including class Clostridia, order Bacillales, and genera Clostridium sensu stricto 1, Dorea, and Lachnospiraceae UCG001. By contrast, three additional microbial genera (Butyricimonas, Defluviitaleaceae UCG011 and Marvinbryantia) exhibited nominal protective correlations with PD. Cross-cohort analyses further indicated a shared correlation pattern along the Clostridia-Clostridiales-Clostridiaceae/Lachnospiraceae taxonomics potentially linking to PD risk across both discovery and validation cohorts. Mediation analyses indicated that betaine may mediate the Lachnospiraceae UCG001-PD associations, while androstenediol monosulfate may serve as a mediator linking Clostridium sensu stricto 1 to PD. SMR analysis highlights genes like SH2B1, JUP, as key host metabolic genes with potential causal relevance to PD, with colocalization indicating genetic overlaps supporting their potential involvement in gene-microbiota interactions. These findings deepen our understanding of gut-brain axis dysregulation in PD and may provide novel insights for future mechanistic validation and targeted preventive or therapeutic investigations.
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@article {pmid42177729,
year = {2026},
author = {Li, G and Ye, X and Zhou, T and Zhou, Z and Min, Y and Song, H and Liu, X},
title = {Exploratory gut microbiota-host interaction in parkinson's disease: integrative multi-omics analysis of metabolic and epigenetic pathways.},
journal = {AMB Express},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13568-026-02078-6},
pmid = {42177729},
issn = {2191-0855},
support = {PWZxq2022-08//the Key Disciplines Group Construction Project of Pudong Health Bureau of Shanghai/ ; },
abstract = {Mounting evidence has associated gut microbial composition and systemic metabolic profiles with Parkinson's disease (PD), yet causal pathways and molecular mechanisms remain unclear. We employed a systematic two-stage analytical framework integrating multiple Mendelian randomization (MR) approaches, transcriptome and epigenome-wide regulatory analyses, and colocalization analysis to genetically dissect the microbiota-host regulatory network implicated in PD susceptibility. Initially, two-sample MR was performed using gut microbiota data from the MiBioGen consortium, followed by an independent replication MR analysis using mbQTL data from the Dutch Microbiome Project (DMP). The two-step MR approach was employed to identify potential mediation of blood metabolites. Summary data-based MR (SMR) methods were also used to pinpoint key blood metabolic genes and regulatory regions associated with PD risk, with the combination of PD GWAS data, blood expression quantitative trait loci (eQTLs), and DNA methylation quantitative trait loci (mQTLs). Colocalization analyses were performed to explore interactions between host metabolic gene expression and the gut microbiota using blood expression quantitative trait loci (eQTLs) and fecal microbial quantitative trait loci (mbQTLs). Our multi-stage analyses identified five microbial taxa with nominal positive associations with Parkinson's disease (PD), including class Clostridia, order Bacillales, and genera Clostridium sensu stricto 1, Dorea, and Lachnospiraceae UCG001. By contrast, three additional microbial genera (Butyricimonas, Defluviitaleaceae UCG011 and Marvinbryantia) exhibited nominal protective correlations with PD. Cross-cohort analyses further indicated a shared correlation pattern along the Clostridia-Clostridiales-Clostridiaceae/Lachnospiraceae taxonomics potentially linking to PD risk across both discovery and validation cohorts. Mediation analyses indicated that betaine may mediate the Lachnospiraceae UCG001-PD associations, while androstenediol monosulfate may serve as a mediator linking Clostridium sensu stricto 1 to PD. SMR analysis highlights genes like SH2B1, JUP, as key host metabolic genes with potential causal relevance to PD, with colocalization indicating genetic overlaps supporting their potential involvement in gene-microbiota interactions. These findings deepen our understanding of gut-brain axis dysregulation in PD and may provide novel insights for future mechanistic validation and targeted preventive or therapeutic investigations.},
}
RevDate: 2026-05-24
CmpDate: 2026-05-24
The epigenetic archaeology of human-dog companionship.
Epigenetics, 21(1):2676911.
Humans have coexisted with dogs for at least 20,000 years, yet the biological consequences of long-term human-dog co-residence remain poorly understood. We propose that sustained exposure to dogs may have contributed to context-dependent variation in human stress regulation, immune function, and socio-emotional neurobiology through environmentally responsive epigenetic mechanisms. Here, we define an epigenetic imprint as detectable differences in gene-regulatory marks, including DNA methylation at environmentally sensitive loci, consistent with developmental plasticity and early-life environmental calibration rather than germline inheritance. In this Commentary, we integrate evidence from genomics, neuroscience, microbiome research, evolutionary anthropology, and palaeoepigenetics to examine whether multispecies living environments may represent an under-recognised biological exposure shaping human regulatory biology. We further outline a framework to test whether archaeologically inferred dog co-residence is associated with epigenetic and regulatory signatures in ancient human populations while accounting for major ecological and demographic confounds. Overall, we argue that human-dog cohabitation provides a plausible and testable model for investigating how long-term social and ecological relationships may influence stress and immune regulation across populations.
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@article {pmid42177806,
year = {2026},
author = {Faraji, J and Metz, GAS},
title = {The epigenetic archaeology of human-dog companionship.},
journal = {Epigenetics},
volume = {21},
number = {1},
pages = {2676911},
doi = {10.1080/15592294.2026.2676911},
pmid = {42177806},
issn = {1559-2308},
mesh = {Humans ; Animals ; *Epigenesis, Genetic ; Dogs ; DNA Methylation ; Archaeology ; *Human-Animal Bond ; },
abstract = {Humans have coexisted with dogs for at least 20,000 years, yet the biological consequences of long-term human-dog co-residence remain poorly understood. We propose that sustained exposure to dogs may have contributed to context-dependent variation in human stress regulation, immune function, and socio-emotional neurobiology through environmentally responsive epigenetic mechanisms. Here, we define an epigenetic imprint as detectable differences in gene-regulatory marks, including DNA methylation at environmentally sensitive loci, consistent with developmental plasticity and early-life environmental calibration rather than germline inheritance. In this Commentary, we integrate evidence from genomics, neuroscience, microbiome research, evolutionary anthropology, and palaeoepigenetics to examine whether multispecies living environments may represent an under-recognised biological exposure shaping human regulatory biology. We further outline a framework to test whether archaeologically inferred dog co-residence is associated with epigenetic and regulatory signatures in ancient human populations while accounting for major ecological and demographic confounds. Overall, we argue that human-dog cohabitation provides a plausible and testable model for investigating how long-term social and ecological relationships may influence stress and immune regulation across populations.},
}
MeSH Terms:
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Humans
Animals
*Epigenesis, Genetic
Dogs
DNA Methylation
Archaeology
*Human-Animal Bond
RevDate: 2026-05-24
Information gain-based molecular ecological network reveals core microbial taxa involved in gastrointestinal recovery following H. pylori infection and intervention with Weizmannia coagulans BC99 in mice.
Microbial pathogenesis, 217:108581 pii:S0882-4010(26)00307-4 [Epub ahead of print].
Helicobacter pylori infection is closely linked to gastric diseases such as ulcers and cancer. Recent studies have suggested that probiotics may help regulate H. pylori-induced dysbiosis. In this study, 25 female C57BL/6 mice were randomly assigned to five groups (n = 5 per group), including a control group, an H. pylori model group, and three BC99 intervention groups receiving low, medium, and high doses, after a 1-week acclimation period. The mice were infected for 1 week and then received BC99 intervention for 4 weeks, examines gastrointestinal microbiome dynamics from infection through recovery following probiotic intervention. A specificity-enhanced, information gain-based molecular ecological network approach was utilized to identify the core microbial taxa in H. pylori-infected mice. We evaluated microbiota restoration, serum inflammatory markers, and digestive enzyme activity utilizing network similarity, linear discriminant analysis, and Euclidean distance metrics for evaluation, followed by causal inference to elucidate microbial interactions. Among the tested groups, high-dose Weizmannia coagulans BC99 exhibited the most pronounced effects. H. pylori primarily disrupted nodes in microbial community 1, while BC99 restored this network structure and promoted microbial balance. Network similarity in the intestine increased from 0.39 to 0.60, and in the stomach it increased from 0.53 to 0.62. Serum indices improved from 0.41 to 0.58, and digestive enzyme activity increased from 0.612 to 0.682. Notably, Lachnospiraceae and Lactobacillaceae exhibited strong causal relationships with H. pylori and Escherichia-Shigella, while Lachnospiraceae and Muribaculaceae were associated with several microbial taxa and physiological indices in the stomach and intestine, respectively. These findings highlight the potential of BC99 in alleviating H. pylori-induced dysbiosis and improving host systemic health, thereby providing a theoretical basis for probiotic-based interventions in gastrointestinal disorders.
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@article {pmid42177863,
year = {2026},
author = {Ye, Y and Jiang, Y and Azeem, S and Zhao, L and Dong, Y and Zhu, J and Fang, S and Wu, Y and Gu, S},
title = {Information gain-based molecular ecological network reveals core microbial taxa involved in gastrointestinal recovery following H. pylori infection and intervention with Weizmannia coagulans BC99 in mice.},
journal = {Microbial pathogenesis},
volume = {217},
number = {},
pages = {108581},
doi = {10.1016/j.micpath.2026.108581},
pmid = {42177863},
issn = {1096-1208},
abstract = {Helicobacter pylori infection is closely linked to gastric diseases such as ulcers and cancer. Recent studies have suggested that probiotics may help regulate H. pylori-induced dysbiosis. In this study, 25 female C57BL/6 mice were randomly assigned to five groups (n = 5 per group), including a control group, an H. pylori model group, and three BC99 intervention groups receiving low, medium, and high doses, after a 1-week acclimation period. The mice were infected for 1 week and then received BC99 intervention for 4 weeks, examines gastrointestinal microbiome dynamics from infection through recovery following probiotic intervention. A specificity-enhanced, information gain-based molecular ecological network approach was utilized to identify the core microbial taxa in H. pylori-infected mice. We evaluated microbiota restoration, serum inflammatory markers, and digestive enzyme activity utilizing network similarity, linear discriminant analysis, and Euclidean distance metrics for evaluation, followed by causal inference to elucidate microbial interactions. Among the tested groups, high-dose Weizmannia coagulans BC99 exhibited the most pronounced effects. H. pylori primarily disrupted nodes in microbial community 1, while BC99 restored this network structure and promoted microbial balance. Network similarity in the intestine increased from 0.39 to 0.60, and in the stomach it increased from 0.53 to 0.62. Serum indices improved from 0.41 to 0.58, and digestive enzyme activity increased from 0.612 to 0.682. Notably, Lachnospiraceae and Lactobacillaceae exhibited strong causal relationships with H. pylori and Escherichia-Shigella, while Lachnospiraceae and Muribaculaceae were associated with several microbial taxa and physiological indices in the stomach and intestine, respectively. These findings highlight the potential of BC99 in alleviating H. pylori-induced dysbiosis and improving host systemic health, thereby providing a theoretical basis for probiotic-based interventions in gastrointestinal disorders.},
}
RevDate: 2026-05-24
Cupuaçu (Theobroma grandiflorum) butter nanoparticles associated with oligosaccharides as cosmetic carriers for prebiotic effect: development, physicochemical characterization, and preclinical evaluation.
European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V pii:S0939-6411(26)00140-2 [Epub ahead of print].
The skin microbiota is essential for cutaneous homeostasis, and prebiotics may support it. Nanostructured systems, such as cupuaçu-derived nanoparticles, enhance the delivery and stability of cosmetic active substances, but their role in modulating the skin microbiota remains unclear and requires targeted evaluation. In this study, lipid-polymeric nanoparticles based on cupuaçu (Theobroma grandiflorum) butter were developed as potential carriers for oligosaccharides. Three formulations were developed: cupuaçu butter (CB-NP), α-glucan oligosaccharide (AGO-CB-NP), and polydextrose nanoparticles (PD-CB-NP). They showed mean diameters of approximately 110 nm, low polydispersity (PdI < 0.30), and moderately negative zeta potentials (around -16 mV). Rheology demonstrated pseudoplastic behavior. Structural characterization by X-ray diffraction (XRD), differential scanning calorimetry (DSC), Fourier-transform infrared spectroscopy (FTIR), transmission electron microscopy (TEM), and small-angle X-ray scattering (SAXS) indicated reduced crystallinity, chemical compatibility among the ingredients, and a hybrid core-shell organization, with a lipid-rich inner region and an outer layer likely associated with oligosaccharides. The formulations exhibited neither eye irritation nor phototoxicity potential in toxicological screening, conducted in accordance with OECD TG 491 and TG 432. In vitro prebiotic potential showed species-dependent responses: AGO-CB-NP stimulated the mutualist Staphylococcus epidermidis while inhibiting Malassezia furfur, whereas CB-NP inhibited Candida albicans growth. Moderate antioxidant activity (around 20% DPPH scavenging) was observed, and cupuaçu butter contained low levels of phenolic compounds (around 0.12 mg GAE g[-1]) and intermediate protection against UVA-induced reactive oxygen species. Among the tested formulations, AGO-CB-NP showed the most favorable overall profile. Overall, the results suggest a promising strategy for developing carriers for microbiome-oriented cosmetic formulations, encouraging further investigation in more complex biological systems, such as in clinical trials.
Additional Links: PMID-42178033
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@article {pmid42178033,
year = {2026},
author = {Fiod Riccioa, BV and Debiasi, BW and de Jesus da Silva, I and Tonani, L and Dos Santos Cunha Chellegatti, MA and Jacometti Cardoso Furtado, NA and von Zeska Kress, MR and Badra Lopes Bentley, MV and Gaspar, LR},
title = {Cupuaçu (Theobroma grandiflorum) butter nanoparticles associated with oligosaccharides as cosmetic carriers for prebiotic effect: development, physicochemical characterization, and preclinical evaluation.},
journal = {European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V},
volume = {},
number = {},
pages = {115119},
doi = {10.1016/j.ejpb.2026.115119},
pmid = {42178033},
issn = {1873-3441},
abstract = {The skin microbiota is essential for cutaneous homeostasis, and prebiotics may support it. Nanostructured systems, such as cupuaçu-derived nanoparticles, enhance the delivery and stability of cosmetic active substances, but their role in modulating the skin microbiota remains unclear and requires targeted evaluation. In this study, lipid-polymeric nanoparticles based on cupuaçu (Theobroma grandiflorum) butter were developed as potential carriers for oligosaccharides. Three formulations were developed: cupuaçu butter (CB-NP), α-glucan oligosaccharide (AGO-CB-NP), and polydextrose nanoparticles (PD-CB-NP). They showed mean diameters of approximately 110 nm, low polydispersity (PdI < 0.30), and moderately negative zeta potentials (around -16 mV). Rheology demonstrated pseudoplastic behavior. Structural characterization by X-ray diffraction (XRD), differential scanning calorimetry (DSC), Fourier-transform infrared spectroscopy (FTIR), transmission electron microscopy (TEM), and small-angle X-ray scattering (SAXS) indicated reduced crystallinity, chemical compatibility among the ingredients, and a hybrid core-shell organization, with a lipid-rich inner region and an outer layer likely associated with oligosaccharides. The formulations exhibited neither eye irritation nor phototoxicity potential in toxicological screening, conducted in accordance with OECD TG 491 and TG 432. In vitro prebiotic potential showed species-dependent responses: AGO-CB-NP stimulated the mutualist Staphylococcus epidermidis while inhibiting Malassezia furfur, whereas CB-NP inhibited Candida albicans growth. Moderate antioxidant activity (around 20% DPPH scavenging) was observed, and cupuaçu butter contained low levels of phenolic compounds (around 0.12 mg GAE g[-1]) and intermediate protection against UVA-induced reactive oxygen species. Among the tested formulations, AGO-CB-NP showed the most favorable overall profile. Overall, the results suggest a promising strategy for developing carriers for microbiome-oriented cosmetic formulations, encouraging further investigation in more complex biological systems, such as in clinical trials.},
}
RevDate: 2026-05-24
Pre-existing liver dysfunction modulates di-(2-ethylhexyl) phthalate (DEHP)-associated biological responses through host-microbiome networks.
Environmental pollution (Barking, Essex : 1987) pii:S0269-7491(26)00787-6 [Epub ahead of print].
Pre-existing metabolic conditions may profoundly alter biological responses to environmental pollutants, yet this dimension remains underexplored in environmental health. This study examined whether pre-existing metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with altered biological responses to di-(2-ethylhexyl) phthalate (DEHP), a ubiquitous plasticizer. In a human cohort, fatty liver status was associated with altered urinary DEHP metabolite profiles, characterized by a higher proportion of the bioactive mono-(2-ethylhexyl) phthalate, suggesting disease-associated differences in DEHP biotransformation. Using a rat model and multi-omics approaches, we observed that hepatic lipid accumulation was associated with higher systemic DEHP burden and altered tissue distribution, with increased accumulation in the liver and intestine. Under this dual stress, DEHP exposure was associated with perturbations in key metabolic pathways, including amino acid, lipid, and drug metabolism. Transcriptomic analysis revealed upregulation of genes involved in fatty acid synthesis and cholesterol metabolism, consistent with enhanced hepatic lipogenesis. Concurrently, gut microbiota dysbiosis intensified, characterized by shifts in microbial community composition, including reduced Firmicutes and Bacteroidota and altered genus-level taxa linked to host metabolic and inflammatory responses. Integrative multi-omics analysis indicated possible coordinated alterations across the microbiome, metabolome, and hepatic transcriptome, potentially involving lipid metabolism and inflammatory signaling pathways. Taken together, these findings suggest that pre-existing MASLD may exacerbate DEHP-associated biological responses through pathways involving the gut-liver axis, highlighting host metabolic status as an important consideration in interpreting chemical-associated biological responses.
Additional Links: PMID-42178099
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@article {pmid42178099,
year = {2026},
author = {Wu, M and Chen, S and Guo, W and Gu, S and Li, K and Shi, Y and Qian, Y and Sun, Y and Liu, Y and Zhu, H},
title = {Pre-existing liver dysfunction modulates di-(2-ethylhexyl) phthalate (DEHP)-associated biological responses through host-microbiome networks.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {128417},
doi = {10.1016/j.envpol.2026.128417},
pmid = {42178099},
issn = {1873-6424},
abstract = {Pre-existing metabolic conditions may profoundly alter biological responses to environmental pollutants, yet this dimension remains underexplored in environmental health. This study examined whether pre-existing metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with altered biological responses to di-(2-ethylhexyl) phthalate (DEHP), a ubiquitous plasticizer. In a human cohort, fatty liver status was associated with altered urinary DEHP metabolite profiles, characterized by a higher proportion of the bioactive mono-(2-ethylhexyl) phthalate, suggesting disease-associated differences in DEHP biotransformation. Using a rat model and multi-omics approaches, we observed that hepatic lipid accumulation was associated with higher systemic DEHP burden and altered tissue distribution, with increased accumulation in the liver and intestine. Under this dual stress, DEHP exposure was associated with perturbations in key metabolic pathways, including amino acid, lipid, and drug metabolism. Transcriptomic analysis revealed upregulation of genes involved in fatty acid synthesis and cholesterol metabolism, consistent with enhanced hepatic lipogenesis. Concurrently, gut microbiota dysbiosis intensified, characterized by shifts in microbial community composition, including reduced Firmicutes and Bacteroidota and altered genus-level taxa linked to host metabolic and inflammatory responses. Integrative multi-omics analysis indicated possible coordinated alterations across the microbiome, metabolome, and hepatic transcriptome, potentially involving lipid metabolism and inflammatory signaling pathways. Taken together, these findings suggest that pre-existing MASLD may exacerbate DEHP-associated biological responses through pathways involving the gut-liver axis, highlighting host metabolic status as an important consideration in interpreting chemical-associated biological responses.},
}
RevDate: 2026-05-24
CmpDate: 2026-05-24
Research on gut microbiota and metabolic characteristics in patients with sleep disorders after ischemic stroke.
Metabolic brain disease, 41(1):.
Post-stroke sleep disorder (PSSD) is a common but underrecognized complication of ischemic stroke, affecting neurological recovery and quality of life. Emerging evidence suggests a role for the gut-brain axis (GBA) in regulating sleep and post-stroke inflammation, yet the microbiome and metabolomic signatures of PSSD remain poorly defined. This study aimed to characterize the gut microbiota and metabolic profiles of PSSD patients, identify potential biomarkers, and explore potential microbial-metabolite-clinical associations. A total of 42 ischemic stroke patients (17 with PSSD, 25 without) and 23 healthy controls were enrolled. Sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI). Fecal samples were analyzed by 16 S rDNA sequencing and untargeted metabolomics, and KEGG pathway enrichment were used to integrate multi-omic data and clinical parameters. Age and serum lymphocyte levels were independent risk factors for PSSD. PSSD patients exhibited enriched pro-inflammatory genera such as Veillonella and Citrobacter. Metabolomic profiling demonstrated elevated histamine and hesperetin in PSSD, along with decreased 6-Dimethylaminopurine and LysoPE(0:0/18:3). Integrated microbiota-metabolite-host analyses revealed correlations between differential taxa, metabolites, and clinical indices, including PSQI scores, HDL-C, and inflammatory markers. Our findings indicate that PSSD is associated with a distinct gut microbial and metabolic signature, highlighting potential mechanistic links through neuroinflammation, neurotransmitter imbalance, and disrupted energy metabolism. These results provide a foundation for developing gut-targeted biomarkers and therapeutic strategies for post-stroke sleep disorders.
Additional Links: PMID-42178430
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@article {pmid42178430,
year = {2026},
author = {Chen, Z and Bao, W and Su, J and Wu, X and Tan, X and Yang, X},
title = {Research on gut microbiota and metabolic characteristics in patients with sleep disorders after ischemic stroke.},
journal = {Metabolic brain disease},
volume = {41},
number = {1},
pages = {},
pmid = {42178430},
issn = {1573-7365},
support = {82302852//National Natural Science Foundation of China/ ; 2021YFA1301102//National Key Research and Development Program of China/ ; 2024E10108//Zhejiang Key Laboratory of Intelligent Rehabilitation and Translational Neuroelectronics/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Male ; Female ; Middle Aged ; *Ischemic Stroke/complications/metabolism/microbiology ; Aged ; *Sleep Wake Disorders/metabolism/etiology/microbiology ; Metabolomics/methods ; },
abstract = {Post-stroke sleep disorder (PSSD) is a common but underrecognized complication of ischemic stroke, affecting neurological recovery and quality of life. Emerging evidence suggests a role for the gut-brain axis (GBA) in regulating sleep and post-stroke inflammation, yet the microbiome and metabolomic signatures of PSSD remain poorly defined. This study aimed to characterize the gut microbiota and metabolic profiles of PSSD patients, identify potential biomarkers, and explore potential microbial-metabolite-clinical associations. A total of 42 ischemic stroke patients (17 with PSSD, 25 without) and 23 healthy controls were enrolled. Sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI). Fecal samples were analyzed by 16 S rDNA sequencing and untargeted metabolomics, and KEGG pathway enrichment were used to integrate multi-omic data and clinical parameters. Age and serum lymphocyte levels were independent risk factors for PSSD. PSSD patients exhibited enriched pro-inflammatory genera such as Veillonella and Citrobacter. Metabolomic profiling demonstrated elevated histamine and hesperetin in PSSD, along with decreased 6-Dimethylaminopurine and LysoPE(0:0/18:3). Integrated microbiota-metabolite-host analyses revealed correlations between differential taxa, metabolites, and clinical indices, including PSQI scores, HDL-C, and inflammatory markers. Our findings indicate that PSSD is associated with a distinct gut microbial and metabolic signature, highlighting potential mechanistic links through neuroinflammation, neurotransmitter imbalance, and disrupted energy metabolism. These results provide a foundation for developing gut-targeted biomarkers and therapeutic strategies for post-stroke sleep disorders.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome/physiology
Male
Female
Middle Aged
*Ischemic Stroke/complications/metabolism/microbiology
Aged
*Sleep Wake Disorders/metabolism/etiology/microbiology
Metabolomics/methods
RevDate: 2026-05-24
Engineering microbial symbiosis and dysbiosis reveals a new AhR-mediated mechanism underlying dandruff pathogenesis.
The British journal of dermatology pii:8691856 [Epub ahead of print].
BACKGROUND: The skin microbiome plays a pivotal role in regulating epidermal barrier integrity and immune homeostasis. However, the molecular mechanisms through which microbial dysbiosis drives dermatological disease and in particular, the pathways by which alterations in the scalp microbiome give rise to the pathological features of dandruff are not fully understood.
OBJECTIVES: This study aimed to establish and validate microbially colonised, full-thickness human skin equivalents (HSEs) that incorporate scalp-relevant bacterial and fungal microbiome species, to dissect the molecular pathways linking microbiome composition to epidermal morphology, barrier function and skin homeostasis.
METHODS: We engineered HSEs colonised with microbial consortia representing healthy (5M) and dandruff-associated (5MP) scalp microbiomes. Morphological and histological analyses were used to assess epidermal architecture and barrier integrity. Expression of key barrier proteins and enzymes involved in corneodesmosome hydrolysis was quantified. Bulk RNA-sequencing was performed to identify differentially regulated signalling pathways, followed by protein validation using immunofluorescence analysis. Key findings were further corroborated with human scalp biopsy specimens from individuals with and without dandruff.
RESULTS: HSEs colonised with the 5M microbiome maintained normal epidermal morphology and expression of barrier-associated proteins. In contrast, HSEs colonised with the 5MP microbiome developed hallmark dandruff-like phenotypes, including altered epidermal morphology, reduced barrier protein expression, and abnormal corneodesmosome degradation. Transcriptomic analysis and protein validation revealed significant attenuation of the aryl hydrocarbon receptor (AhR) signalling pathway in 5MP-colonised HSEs. Consistent downregulation of AhR and associated proteins was observed in dandruff patient samples, confirming the clinical relevance.
CONCLUSIONS: Microbial dysbiosis on the scalp can compromise AhR signalling. This study provides mechanistic evidence linking microbiome composition to pathological epidermal changes. The developed microbially colonised HSE model provides a versatile and clinically relevant tool for advancing our understanding of microbiome-driven skin pathology and translating mechanistic insights into precision interventions.
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@article {pmid42178487,
year = {2026},
author = {McPolin-Hall, E and Stephen, AS and Pardieu, C and Georgeu, G and Allaker, RP and Bhogal, RK and Pople, JE and Philpott, MP and Hannen, RF},
title = {Engineering microbial symbiosis and dysbiosis reveals a new AhR-mediated mechanism underlying dandruff pathogenesis.},
journal = {The British journal of dermatology},
volume = {},
number = {},
pages = {},
doi = {10.1093/bjd/ljag210},
pmid = {42178487},
issn = {1365-2133},
abstract = {BACKGROUND: The skin microbiome plays a pivotal role in regulating epidermal barrier integrity and immune homeostasis. However, the molecular mechanisms through which microbial dysbiosis drives dermatological disease and in particular, the pathways by which alterations in the scalp microbiome give rise to the pathological features of dandruff are not fully understood.
OBJECTIVES: This study aimed to establish and validate microbially colonised, full-thickness human skin equivalents (HSEs) that incorporate scalp-relevant bacterial and fungal microbiome species, to dissect the molecular pathways linking microbiome composition to epidermal morphology, barrier function and skin homeostasis.
METHODS: We engineered HSEs colonised with microbial consortia representing healthy (5M) and dandruff-associated (5MP) scalp microbiomes. Morphological and histological analyses were used to assess epidermal architecture and barrier integrity. Expression of key barrier proteins and enzymes involved in corneodesmosome hydrolysis was quantified. Bulk RNA-sequencing was performed to identify differentially regulated signalling pathways, followed by protein validation using immunofluorescence analysis. Key findings were further corroborated with human scalp biopsy specimens from individuals with and without dandruff.
RESULTS: HSEs colonised with the 5M microbiome maintained normal epidermal morphology and expression of barrier-associated proteins. In contrast, HSEs colonised with the 5MP microbiome developed hallmark dandruff-like phenotypes, including altered epidermal morphology, reduced barrier protein expression, and abnormal corneodesmosome degradation. Transcriptomic analysis and protein validation revealed significant attenuation of the aryl hydrocarbon receptor (AhR) signalling pathway in 5MP-colonised HSEs. Consistent downregulation of AhR and associated proteins was observed in dandruff patient samples, confirming the clinical relevance.
CONCLUSIONS: Microbial dysbiosis on the scalp can compromise AhR signalling. This study provides mechanistic evidence linking microbiome composition to pathological epidermal changes. The developed microbially colonised HSE model provides a versatile and clinically relevant tool for advancing our understanding of microbiome-driven skin pathology and translating mechanistic insights into precision interventions.},
}
RevDate: 2026-05-24
CmpDate: 2026-05-25
Ammonia oxidation and recalcitrant carbon degradation fuel mixotrophic growth in the symbiont community of a deep-sea sponge.
Microbiome, 14(1):.
BACKGROUND: Sponges are important members of shallow-water, benthic ecosystems, where they often rely on their microbial symbionts to acquire organic or inorganic carbon. Sponges are also found in the deep sea, however, how they metabolically interact there with their symbionts remains underexplored. Here, we combined metagenomic, metatranscriptomic and stable-isotope labelling approaches to investigate the metabolic activities of the microbial community of the deep-sea sponge Calyx sp.
RESULTS: Approximately 84% of the total estimated microbial abundance was composed of nine heterotrophic phyla, whilst the remaining 16% consisted of two autotrophic ammonia-oxidising archaea. Metatranscriptomic analysis revealed the high expression of genes involved in the degradation of recalcitrant polysaccharides of algal origin, suggesting that an undegraded fraction of marine snow plays a role in the nutrition of this deep-sea holobiont. Additionally, we detected active ammonia oxidation and carbon fixation pathways in the autotrophic community members and, through ex situ incubations with labelled carbonate show a potential to fix 13.67 mg CO2 per g dry weight in a year.
CONCLUSIONS: This study highlights the mixotrophic lifestyle of a deep-sea sponge microbiome, expanding our knowledge of the sponge-microbe symbiosis in the oligotrophic environment of the deep ocean. Video Abstract.
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@article {pmid42178569,
year = {2026},
author = {Garritano, AN and J Hill, L and Ribeiro, B and Damasceno, T and Medeiros, L and Duarte, G and L S Vilela, C and Majzoub, ME and Allen, MA and Nappi, J and S Peixoto, R and Thomas, T},
title = {Ammonia oxidation and recalcitrant carbon degradation fuel mixotrophic growth in the symbiont community of a deep-sea sponge.},
journal = {Microbiome},
volume = {14},
number = {1},
pages = {},
pmid = {42178569},
issn = {2049-2618},
support = {BAS/1/1095-01-01//KAUST/ ; ANP 21005-4//ANP, Brazil/ ; },
mesh = {Animals ; *Porifera/microbiology ; *Ammonia/metabolism ; *Symbiosis ; Oxidation-Reduction ; *Archaea/metabolism/genetics/classification/isolation & purification ; *Microbiota ; *Carbon/metabolism ; *Bacteria/classification/metabolism/genetics/isolation & purification ; Metagenomics/methods ; Autotrophic Processes ; Carbon Cycle ; Seawater/microbiology ; },
abstract = {BACKGROUND: Sponges are important members of shallow-water, benthic ecosystems, where they often rely on their microbial symbionts to acquire organic or inorganic carbon. Sponges are also found in the deep sea, however, how they metabolically interact there with their symbionts remains underexplored. Here, we combined metagenomic, metatranscriptomic and stable-isotope labelling approaches to investigate the metabolic activities of the microbial community of the deep-sea sponge Calyx sp.
RESULTS: Approximately 84% of the total estimated microbial abundance was composed of nine heterotrophic phyla, whilst the remaining 16% consisted of two autotrophic ammonia-oxidising archaea. Metatranscriptomic analysis revealed the high expression of genes involved in the degradation of recalcitrant polysaccharides of algal origin, suggesting that an undegraded fraction of marine snow plays a role in the nutrition of this deep-sea holobiont. Additionally, we detected active ammonia oxidation and carbon fixation pathways in the autotrophic community members and, through ex situ incubations with labelled carbonate show a potential to fix 13.67 mg CO2 per g dry weight in a year.
CONCLUSIONS: This study highlights the mixotrophic lifestyle of a deep-sea sponge microbiome, expanding our knowledge of the sponge-microbe symbiosis in the oligotrophic environment of the deep ocean. Video Abstract.},
}
MeSH Terms:
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hide MeSH Terms
Animals
*Porifera/microbiology
*Ammonia/metabolism
*Symbiosis
Oxidation-Reduction
*Archaea/metabolism/genetics/classification/isolation & purification
*Microbiota
*Carbon/metabolism
*Bacteria/classification/metabolism/genetics/isolation & purification
Metagenomics/methods
Autotrophic Processes
Carbon Cycle
Seawater/microbiology
RevDate: 2026-05-25
The crosslink between autophagy and ferroptosis in polycystic ovary syndrome: from synergistic pathogenesis to targeted therapy.
Journal of ovarian research pii:10.1186/s13048-026-02146-2 [Epub ahead of print].
Polycystic ovary syndrome (PCOS) is a highly heterogeneous endocrine-metabolic disorder whose core pathological features-follicular atresia and ovulatory dysfunction-are attributed to functional failure of ovarian granulosa cells (GCs). Although autophagy (a cellular quality-control mechanism) and ferroptosis (iron-dependent lipid peroxidation-driven cell death) have been shown to independently contribute to the pathophysiology of PCOS, their interactive networks and regulatory mechanisms within specific pathological microenvironments remain to be systematically elucidated. This review aims to systematically unravel this overlooked micro-pathogenic network. The dysfunction of GCs in PCOS is not an isolated event involving a single mode of cell death, but rather a pathological crosstalk arising from the disruption of the dynamic equilibrium between autophagy and ferroptosis. This paper elucidates the pathological mechanisms driving this cascade of disturbances through four distinct pathways: the intracellular stress hub formed by the synergistic action of oxidative stress (OS) and endoplasmic reticulum stress (ERS) serves as the initiating factor. This is compounded by the gut-ovarian axis's long-range amplification effect, mediated by gut microbiome (GM) dysregulation and low-grade chronic inflammation (LGI), collectively disrupting cellular homeostasis. while circadian rhythm disruption and epigenetic reprogramming, respectively, cement this imbalance at the temporal and molecular memory levels. Moreover, we have elucidated the specific execution pathways of autophagy-dependent ferroptosis, namely how selective autophagy (e.g., ferritinophagy and mitophagy) acts as a key amplifier of ferroptosis by exacerbating iron overload and energy collapse. On this basis, this paper explores therapeutic strategies ranging from upstream restoration of signal homeostasis to downstream precise inhibition of autophagy-ferroptosis interaction nodes. This review aims to provide novel theoretical perspectives for fundamentally reversing follicular atresia in PCOS and improving patients' reproductive outcomes by re-examining these lethal interactions at the microscopic level.
Additional Links: PMID-42178591
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@article {pmid42178591,
year = {2026},
author = {Wu, X and Li, J and Zhang, X and Huang, H and Li, T and Kong, M and Dai, Z and Yang, Y and Chen, X},
title = {The crosslink between autophagy and ferroptosis in polycystic ovary syndrome: from synergistic pathogenesis to targeted therapy.},
journal = {Journal of ovarian research},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13048-026-02146-2},
pmid = {42178591},
issn = {1757-2215},
support = {YDZJ202401150ZYTS//Department of Science and Technology of Jilin Province/ ; },
abstract = {Polycystic ovary syndrome (PCOS) is a highly heterogeneous endocrine-metabolic disorder whose core pathological features-follicular atresia and ovulatory dysfunction-are attributed to functional failure of ovarian granulosa cells (GCs). Although autophagy (a cellular quality-control mechanism) and ferroptosis (iron-dependent lipid peroxidation-driven cell death) have been shown to independently contribute to the pathophysiology of PCOS, their interactive networks and regulatory mechanisms within specific pathological microenvironments remain to be systematically elucidated. This review aims to systematically unravel this overlooked micro-pathogenic network. The dysfunction of GCs in PCOS is not an isolated event involving a single mode of cell death, but rather a pathological crosstalk arising from the disruption of the dynamic equilibrium between autophagy and ferroptosis. This paper elucidates the pathological mechanisms driving this cascade of disturbances through four distinct pathways: the intracellular stress hub formed by the synergistic action of oxidative stress (OS) and endoplasmic reticulum stress (ERS) serves as the initiating factor. This is compounded by the gut-ovarian axis's long-range amplification effect, mediated by gut microbiome (GM) dysregulation and low-grade chronic inflammation (LGI), collectively disrupting cellular homeostasis. while circadian rhythm disruption and epigenetic reprogramming, respectively, cement this imbalance at the temporal and molecular memory levels. Moreover, we have elucidated the specific execution pathways of autophagy-dependent ferroptosis, namely how selective autophagy (e.g., ferritinophagy and mitophagy) acts as a key amplifier of ferroptosis by exacerbating iron overload and energy collapse. On this basis, this paper explores therapeutic strategies ranging from upstream restoration of signal homeostasis to downstream precise inhibition of autophagy-ferroptosis interaction nodes. This review aims to provide novel theoretical perspectives for fundamentally reversing follicular atresia in PCOS and improving patients' reproductive outcomes by re-examining these lethal interactions at the microscopic level.},
}
RevDate: 2026-05-25
CmpDate: 2026-05-25
Unraveling Oral Dysbiosis: Microbial Complexity in Common Oral Diseases.
MicrobiologyOpen, 15(3):e70305.
The oral microbiome is highly intricate, hosting billions of bacteria and other microorganisms that form biofilms on various oral surfaces. An imbalanced ecological relationship between the microbial community and the host can lead to various oral diseases. This narrative review explores the current understanding of the correlation between the microbiome and oral diseases. The main body of this manuscript is divided into seven parts, including a review of current research on oral microbial colonization and early life development, an introduction to five common oral diseases related to microorganisms, and a discussion on the relationship between dental caries and periodontal disease at the microbial level. Our aim in presenting this review is to offer a valuable resource for further research on the role of oral microorganisms in diagnosing and treating oral diseases. The oral microbiome's significant impact and diversity characteristics on health and disease have been recognized; however, there remains a severe lack of systematic understanding of its functions, host interactions, and environmental factors. Comprehensive research is urgently needed to elucidate the mechanisms that maintain its ecological balance, providing a scientific foundation for the precise prevention and control of oral diseases. This review comprehensively synthesizes current knowledge regarding oral microbial dysbiosis in the context of the major oral diseases mentioned and proposes a conceptual framework grounded in microbial ecology to elucidate disease progression and guide therapeutic strategies.
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@article {pmid42178691,
year = {2026},
author = {Kang, Z and Huang, H and Lin, J and Niu, Y and Chen, J and Tang, J and Hu, Z and Liu, P and Qu, J},
title = {Unraveling Oral Dysbiosis: Microbial Complexity in Common Oral Diseases.},
journal = {MicrobiologyOpen},
volume = {15},
number = {3},
pages = {e70305},
doi = {10.1002/mbo3.70305},
pmid = {42178691},
issn = {2045-8827},
support = {S202510555045//Hunan Provincial College Students' Innovation and Entrepreneurship Training Program/ ; S202410555239//Hunan Provincial College Students' Innovation and Entrepreneurship Training Program/ ; S202310555226//Hunan Provincial College Students' Innovation and Entrepreneurship Training Program/ ; },
mesh = {*Dysbiosis/microbiology ; Humans ; *Microbiota ; *Mouth/microbiology ; *Mouth Diseases/microbiology ; Periodontal Diseases/microbiology ; Dental Caries/microbiology ; Biofilms/growth & development ; Bacteria/classification/genetics/isolation & purification ; },
abstract = {The oral microbiome is highly intricate, hosting billions of bacteria and other microorganisms that form biofilms on various oral surfaces. An imbalanced ecological relationship between the microbial community and the host can lead to various oral diseases. This narrative review explores the current understanding of the correlation between the microbiome and oral diseases. The main body of this manuscript is divided into seven parts, including a review of current research on oral microbial colonization and early life development, an introduction to five common oral diseases related to microorganisms, and a discussion on the relationship between dental caries and periodontal disease at the microbial level. Our aim in presenting this review is to offer a valuable resource for further research on the role of oral microorganisms in diagnosing and treating oral diseases. The oral microbiome's significant impact and diversity characteristics on health and disease have been recognized; however, there remains a severe lack of systematic understanding of its functions, host interactions, and environmental factors. Comprehensive research is urgently needed to elucidate the mechanisms that maintain its ecological balance, providing a scientific foundation for the precise prevention and control of oral diseases. This review comprehensively synthesizes current knowledge regarding oral microbial dysbiosis in the context of the major oral diseases mentioned and proposes a conceptual framework grounded in microbial ecology to elucidate disease progression and guide therapeutic strategies.},
}
MeSH Terms:
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*Dysbiosis/microbiology
Humans
*Microbiota
*Mouth/microbiology
*Mouth Diseases/microbiology
Periodontal Diseases/microbiology
Dental Caries/microbiology
Biofilms/growth & development
Bacteria/classification/genetics/isolation & purification
RevDate: 2026-05-25
CmpDate: 2026-05-25
Microbiome functional gene pathways are indicative of cognitive performance in older adults at risk for Alzheimer's disease.
Gut microbes, 18(1):2676162.
Disturbances in the gut microbiome are increasingly correlated with neurodegenerative disorders, including Alzheimer's disease. Multiple lines of emerging evidence are consistent with the microbiome's involvement in disease pathology in AD by triggering or potentiating systemic and neuroinflammation, thereby influencing disease pathology through the "microbiota-gut-brain axis." Currently, the copathologies contributing to cognitive decline and symptomatic progression in AD remain unknown and understudied. Changes in the gut microbiome composition may offer clues to potential systemic physiologic and neuropathologic changes that contribute to cognitive decline. Here, we recruited a cohort of 260 older adults (aged 60 y or older) living in the community and followed them over time, tracking objective measures of cognition, clinical information, and gut microbiome samples. Subjects were classified as healthy controls, exhibiting mild cognitive impairment, or having dementia based on clinical assessments. Using metagenomic sequencing and gene pathway analyses, we found that certain microbial-encoded metabolic pathways correlated with worse cognitive performance. Specifically, genes involved in the urea cycle, polyamine synthesis, or the metabolism of methionine and cysteine predicted worse cognitive performance. Our study suggests that the gut microbiome composition may be linked to cognitive impairment along the AD continuum and points to microbial metabolic pathways that may potentiate disease.
Additional Links: PMID-42178714
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PubMed:
Citation:
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@article {pmid42178714,
year = {2026},
author = {Zeamer, AL and Lai, Y and Loew, E and Sanborn, V and Tracy, M and Jo, C and Ferdinand, D and Ward, DV and Bhattarai, SK and Drake, J and McCormick, BA and Bucci, V and Haran, JP},
title = {Microbiome functional gene pathways are indicative of cognitive performance in older adults at risk for Alzheimer's disease.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2676162},
doi = {10.1080/19490976.2026.2676162},
pmid = {42178714},
issn = {1949-0984},
mesh = {Humans ; *Alzheimer Disease/microbiology ; *Gastrointestinal Microbiome/genetics ; Aged ; Female ; Male ; *Cognition ; Middle Aged ; *Cognitive Dysfunction/microbiology ; Aged, 80 and over ; *Bacteria/classification/genetics/isolation & purification/metabolism ; Cohort Studies ; Metagenomics ; Metabolic Networks and Pathways/genetics ; },
abstract = {Disturbances in the gut microbiome are increasingly correlated with neurodegenerative disorders, including Alzheimer's disease. Multiple lines of emerging evidence are consistent with the microbiome's involvement in disease pathology in AD by triggering or potentiating systemic and neuroinflammation, thereby influencing disease pathology through the "microbiota-gut-brain axis." Currently, the copathologies contributing to cognitive decline and symptomatic progression in AD remain unknown and understudied. Changes in the gut microbiome composition may offer clues to potential systemic physiologic and neuropathologic changes that contribute to cognitive decline. Here, we recruited a cohort of 260 older adults (aged 60 y or older) living in the community and followed them over time, tracking objective measures of cognition, clinical information, and gut microbiome samples. Subjects were classified as healthy controls, exhibiting mild cognitive impairment, or having dementia based on clinical assessments. Using metagenomic sequencing and gene pathway analyses, we found that certain microbial-encoded metabolic pathways correlated with worse cognitive performance. Specifically, genes involved in the urea cycle, polyamine synthesis, or the metabolism of methionine and cysteine predicted worse cognitive performance. Our study suggests that the gut microbiome composition may be linked to cognitive impairment along the AD continuum and points to microbial metabolic pathways that may potentiate disease.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Alzheimer Disease/microbiology
*Gastrointestinal Microbiome/genetics
Aged
Female
Male
*Cognition
Middle Aged
*Cognitive Dysfunction/microbiology
Aged, 80 and over
*Bacteria/classification/genetics/isolation & purification/metabolism
Cohort Studies
Metagenomics
Metabolic Networks and Pathways/genetics
RevDate: 2026-05-25
CmpDate: 2026-05-25
Production of Multiple Variants of the Antimicrobial Sactipeptide Gnavucin D by the Human Gut Isolate Mediterraneibacter gnavus HB038.
MicrobiologyOpen, 15(3):e70315.
While several bacteriocins have been identified from gut-isolated cultures, there remains a need for the discovery of bacteriocins with varying inhibition spectra for strain applications such as microbiome editing, pathogen elimination and colonization resistance. With this in mind, here we describe a new antibacterial sactipeptide gnavucin D, produced by Mediterraneibacter gnavus HB038 isolated from a healthy 2-year-old child. Gnavucin D has activity against the pathogens Clostridium perfringens, Streptococcus agalactiae, Bacillus cereus, and vancomycin-resistant Enterococcus. The gene cluster includes five structural genes in tandem that encode for three different core peptides (29 amino acids each) with molecular masses of 2704.21 (D1), 2734.23 (D2/D3), and 2732.21 (D4/D5) Da. The nearest relative to these bacteriocins was found to be another sactipeptide thurincin H produced by Bacillus thuringiensis with which it shares 30% identity. Although the amino acids encoding the gnavucin and thurincin are similar with regard to putative functions, their homology to each other is low, varying from 30% to 55%. Interestingly, all these bacteriocins had short leader peptides of only 9 amino acids. Gnavucin D was found to be extremely stable to temperature, pH and proteolysis which is possibly a reflection of the sulfur to carbon post-translational modifications. The observed molecular masses of the 3 different peptides correspond to four modifications, yielding a structurally restricted, most likely double-hairpin conformation which is characteristic of such sactipeptides. Consequently, gnavucin D can be a promising candidate for selective antibacterial activity against human pathogens.
Additional Links: PMID-42178752
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PubMed:
Citation:
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@article {pmid42178752,
year = {2026},
author = {Ding, M and de Farias, FM and O'Connor, PM and Huang, X and Ross, FC and Kennedy, EC and Hawkes, CP and Hill, C and Stanton, C and Ross, RP},
title = {Production of Multiple Variants of the Antimicrobial Sactipeptide Gnavucin D by the Human Gut Isolate Mediterraneibacter gnavus HB038.},
journal = {MicrobiologyOpen},
volume = {15},
number = {3},
pages = {e70315},
doi = {10.1002/mbo3.70315},
pmid = {42178752},
issn = {2045-8827},
support = {SFI/12/RC/2273//Science Foundation Ireland (SFI)/ ; 101054719//European Union/ ; },
mesh = {Humans ; *Bacteriocins/pharmacology/chemistry/genetics/biosynthesis/metabolism/isolation & purification ; *Eubacteriales/metabolism/isolation & purification/genetics ; Child, Preschool ; *Anti-Bacterial Agents/pharmacology/chemistry/metabolism ; Clostridium perfringens/drug effects ; Bacillus cereus/drug effects ; Multigene Family ; Streptococcus agalactiae/drug effects ; Microbial Sensitivity Tests ; Enterococcus/drug effects ; Gastrointestinal Microbiome ; Amino Acid Sequence ; },
abstract = {While several bacteriocins have been identified from gut-isolated cultures, there remains a need for the discovery of bacteriocins with varying inhibition spectra for strain applications such as microbiome editing, pathogen elimination and colonization resistance. With this in mind, here we describe a new antibacterial sactipeptide gnavucin D, produced by Mediterraneibacter gnavus HB038 isolated from a healthy 2-year-old child. Gnavucin D has activity against the pathogens Clostridium perfringens, Streptococcus agalactiae, Bacillus cereus, and vancomycin-resistant Enterococcus. The gene cluster includes five structural genes in tandem that encode for three different core peptides (29 amino acids each) with molecular masses of 2704.21 (D1), 2734.23 (D2/D3), and 2732.21 (D4/D5) Da. The nearest relative to these bacteriocins was found to be another sactipeptide thurincin H produced by Bacillus thuringiensis with which it shares 30% identity. Although the amino acids encoding the gnavucin and thurincin are similar with regard to putative functions, their homology to each other is low, varying from 30% to 55%. Interestingly, all these bacteriocins had short leader peptides of only 9 amino acids. Gnavucin D was found to be extremely stable to temperature, pH and proteolysis which is possibly a reflection of the sulfur to carbon post-translational modifications. The observed molecular masses of the 3 different peptides correspond to four modifications, yielding a structurally restricted, most likely double-hairpin conformation which is characteristic of such sactipeptides. Consequently, gnavucin D can be a promising candidate for selective antibacterial activity against human pathogens.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Bacteriocins/pharmacology/chemistry/genetics/biosynthesis/metabolism/isolation & purification
*Eubacteriales/metabolism/isolation & purification/genetics
Child, Preschool
*Anti-Bacterial Agents/pharmacology/chemistry/metabolism
Clostridium perfringens/drug effects
Bacillus cereus/drug effects
Multigene Family
Streptococcus agalactiae/drug effects
Microbial Sensitivity Tests
Enterococcus/drug effects
Gastrointestinal Microbiome
Amino Acid Sequence
RevDate: 2026-05-25
CmpDate: 2026-05-25
Shared Secondary Metabolites Between Salicornia brachiata and Its Bacillus Endophytes Reveal a Cooperative Chemical Defense.
Chemistry & biodiversity, 23(5):e71352.
This study explores the chemical ecology of the halophytic plant Salicornia brachiata and its associated Bacillus endophytes using LC-MS-based metabolomics. A total of 43 Bacillus strains were isolated and screened for the production of bioactive lipopeptides, with 26 strains showing both lipopeptide production and antimicrobial activity, particularly against Mycobacterium smegmatis MTCC6. Fermentation of a potent endophyte, Bacillus subtilis NPRoot-3, yielded purified surfactins and fengycins, which displayed significant inhibitory activity with low IC50 values against Mycobacterium smegmatis. LC-MS analysis of aqueous and methanolic extracts of S. brachiata revealed molecular features putatively corresponding to surfactins, fengycins, and bacillibactins, indicating the presence of similar bioactive compounds in both the host plant and its endophytic microbiome. These findings suggest that the antimycobacterial properties of S. brachiata may be partly attributed to metabolites produced by its endophytes. Overall, this study highlights cooperative defense mechanisms between the plant and its endophytes, confirms the role of endophyte-derived secondary metabolites in shaping plant bioactivity and offers promising leads for the discovery of novel antimycobacterial agents.
Additional Links: PMID-42178807
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PubMed:
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@article {pmid42178807,
year = {2026},
author = {Singh, S and Nalli, Y and Krishan, and Gajjar, A and Shinde, UP and Shinde, PB},
title = {Shared Secondary Metabolites Between Salicornia brachiata and Its Bacillus Endophytes Reveal a Cooperative Chemical Defense.},
journal = {Chemistry & biodiversity},
volume = {23},
number = {5},
pages = {e71352},
doi = {10.1002/cbdv.71352},
pmid = {42178807},
issn = {1612-1880},
support = {ECRA/2016/000788//Department of Science and Technology/ ; //Scientific and Engineering Research Board (SERB)/ ; MLP/0027//Council of Scientific and Industrial Research/ ; MLP/0027//Council of Scientific and Industrial Research/ ; },
mesh = {*Chenopodiaceae/metabolism/chemistry/microbiology ; *Endophytes/metabolism/chemistry ; *Bacillus/metabolism/chemistry ; *Anti-Bacterial Agents/pharmacology/chemistry/isolation & purification/metabolism ; Microbial Sensitivity Tests ; Mycobacterium smegmatis/drug effects ; Secondary Metabolism ; *Lipopeptides/pharmacology/chemistry/isolation & purification/metabolism ; },
abstract = {This study explores the chemical ecology of the halophytic plant Salicornia brachiata and its associated Bacillus endophytes using LC-MS-based metabolomics. A total of 43 Bacillus strains were isolated and screened for the production of bioactive lipopeptides, with 26 strains showing both lipopeptide production and antimicrobial activity, particularly against Mycobacterium smegmatis MTCC6. Fermentation of a potent endophyte, Bacillus subtilis NPRoot-3, yielded purified surfactins and fengycins, which displayed significant inhibitory activity with low IC50 values against Mycobacterium smegmatis. LC-MS analysis of aqueous and methanolic extracts of S. brachiata revealed molecular features putatively corresponding to surfactins, fengycins, and bacillibactins, indicating the presence of similar bioactive compounds in both the host plant and its endophytic microbiome. These findings suggest that the antimycobacterial properties of S. brachiata may be partly attributed to metabolites produced by its endophytes. Overall, this study highlights cooperative defense mechanisms between the plant and its endophytes, confirms the role of endophyte-derived secondary metabolites in shaping plant bioactivity and offers promising leads for the discovery of novel antimycobacterial agents.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Chenopodiaceae/metabolism/chemistry/microbiology
*Endophytes/metabolism/chemistry
*Bacillus/metabolism/chemistry
*Anti-Bacterial Agents/pharmacology/chemistry/isolation & purification/metabolism
Microbial Sensitivity Tests
Mycobacterium smegmatis/drug effects
Secondary Metabolism
*Lipopeptides/pharmacology/chemistry/isolation & purification/metabolism
RevDate: 2026-05-25
Effects of Human Lactoferrin (Effera[®]) at Two Doses Versus Bovine Lactoferrin on the Adult Gut Microbiome and Fecal Short-Chain Fatty Acids: a Randomized, Double-Blind Trial.
Journal of dietary supplements [Epub ahead of print].
Human lactoferrin (hLF) is a glycoprotein of commercial interest as a food ingredient for gut health. We conducted an exploratory analysis comparing the effects of Helaina hLF (effera[®]), produced by Komagataella phaffii, and bovine LF (bLF) on the adult gut microbiome and fecal metabolites. In a randomized, double-blind, parallel-arm, controlled trial, 66 healthy adults received either high-dose (HD) effera[®] (3.4 g/day), low-dose (LD) effera[®] (0.34 g/day), or bLF (3.4 g/day) supplementation for 28 days. Fecal samples collected at Days 0 (baseline), 28, 56, and 84 were analyzed for microbial diversity, taxonomic shifts, and volatile fatty acids (VFA). Alpha-diversity remained stable across all groups. Beta-diversity showed no main effect of treatment; however, bLF was associated with significant visit-related shifts, as assessed by weighted UniFrac. At the phylum level, significant changes associated with effera[®] were observed, including decreases in Bacillota (LD) and Verrucomicrobiota (HD), and notable genus-level increases in Lachnospira, Paraprevotella, and Faecalibacterium (HD), while bLF was associated with an increase Bacteroidota at the phylum level and with an increase in the genus Roseburia. Both effera[®] and bLF were associated with decreases in Blautia and Dorea. VFA analysis revealed that bLF increased absolute concentrations of total short-chain fatty acids (SCFAs) and branched-chain fatty acids (BCFAs); both effera[®] treatments produced proportional changes in SCFAs as a percent of total VFA, acetate, and individual BCFAs. In healthy adults, effera[®] supplementation promoted a proportional increase in acetate and supported potentially beneficial taxa while maintaining microbial diversity, without disrupting community structure. As a pre-specified exploratory outcome, microbiome and VFA findings should be interpreted as hypothesis-generating. (clinicaltrials.gov: NCT06012669).
Additional Links: PMID-42178844
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PubMed:
Citation:
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@article {pmid42178844,
year = {2026},
author = {Peterson, RD and van der Made, J and Donovan, SM and Wang, M and Dilger, RN and Kaplan, N and Clark, AJ},
title = {Effects of Human Lactoferrin (Effera[®]) at Two Doses Versus Bovine Lactoferrin on the Adult Gut Microbiome and Fecal Short-Chain Fatty Acids: a Randomized, Double-Blind Trial.},
journal = {Journal of dietary supplements},
volume = {},
number = {},
pages = {1-25},
doi = {10.1080/19390211.2026.2673021},
pmid = {42178844},
issn = {1939-022X},
abstract = {Human lactoferrin (hLF) is a glycoprotein of commercial interest as a food ingredient for gut health. We conducted an exploratory analysis comparing the effects of Helaina hLF (effera[®]), produced by Komagataella phaffii, and bovine LF (bLF) on the adult gut microbiome and fecal metabolites. In a randomized, double-blind, parallel-arm, controlled trial, 66 healthy adults received either high-dose (HD) effera[®] (3.4 g/day), low-dose (LD) effera[®] (0.34 g/day), or bLF (3.4 g/day) supplementation for 28 days. Fecal samples collected at Days 0 (baseline), 28, 56, and 84 were analyzed for microbial diversity, taxonomic shifts, and volatile fatty acids (VFA). Alpha-diversity remained stable across all groups. Beta-diversity showed no main effect of treatment; however, bLF was associated with significant visit-related shifts, as assessed by weighted UniFrac. At the phylum level, significant changes associated with effera[®] were observed, including decreases in Bacillota (LD) and Verrucomicrobiota (HD), and notable genus-level increases in Lachnospira, Paraprevotella, and Faecalibacterium (HD), while bLF was associated with an increase Bacteroidota at the phylum level and with an increase in the genus Roseburia. Both effera[®] and bLF were associated with decreases in Blautia and Dorea. VFA analysis revealed that bLF increased absolute concentrations of total short-chain fatty acids (SCFAs) and branched-chain fatty acids (BCFAs); both effera[®] treatments produced proportional changes in SCFAs as a percent of total VFA, acetate, and individual BCFAs. In healthy adults, effera[®] supplementation promoted a proportional increase in acetate and supported potentially beneficial taxa while maintaining microbial diversity, without disrupting community structure. As a pre-specified exploratory outcome, microbiome and VFA findings should be interpreted as hypothesis-generating. (clinicaltrials.gov: NCT06012669).},
}
RevDate: 2026-05-25
CmpDate: 2026-05-25
Oxysterol Signaling Within the Microbiome-Regulated Gut-Liver-Brain Axis: Implications for Metabolic Homeostasis and Neurodegeneration.
Comprehensive Physiology, 16(3):e70181.
The gut-liver-brain axis integrates metabolic and inflammatory signals that influence systemic homeostasis and cognitive function. While current models emphasize short-chain fatty acids and bile acids, they do not fully explain lipid-driven neurodegenerative processes. Oxysterols, oxidized derivatives of cholesterol, are emerging as key signaling molecules that bridge peripheral metabolism and brain function. Generated at the gut-liver interface through enzymatic and oxidative pathways, oxysterols regulate lipid and glucose metabolism via nuclear receptors, including liver X receptors and farnesoid X receptor. Importantly, specific oxysterols cross the blood brain barrier, enabling bidirectional communication between the periphery and central nervous system. By modulating neuroinflammation and synaptic function, oxysterols provide a mechanistic link between metabolic dysfunction and cognitive decline.
Additional Links: PMID-42178901
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PubMed:
Citation:
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@article {pmid42178901,
year = {2026},
author = {Ganamurali, N and Sabarathinam, S},
title = {Oxysterol Signaling Within the Microbiome-Regulated Gut-Liver-Brain Axis: Implications for Metabolic Homeostasis and Neurodegeneration.},
journal = {Comprehensive Physiology},
volume = {16},
number = {3},
pages = {e70181},
doi = {10.1002/cph4.70181},
pmid = {42178901},
issn = {2040-4603},
mesh = {Humans ; *Oxysterols/metabolism ; Animals ; *Gastrointestinal Microbiome/physiology ; *Brain/metabolism ; Homeostasis/physiology ; *Liver/metabolism ; Signal Transduction/physiology ; *Neurodegenerative Diseases/metabolism ; },
abstract = {The gut-liver-brain axis integrates metabolic and inflammatory signals that influence systemic homeostasis and cognitive function. While current models emphasize short-chain fatty acids and bile acids, they do not fully explain lipid-driven neurodegenerative processes. Oxysterols, oxidized derivatives of cholesterol, are emerging as key signaling molecules that bridge peripheral metabolism and brain function. Generated at the gut-liver interface through enzymatic and oxidative pathways, oxysterols regulate lipid and glucose metabolism via nuclear receptors, including liver X receptors and farnesoid X receptor. Importantly, specific oxysterols cross the blood brain barrier, enabling bidirectional communication between the periphery and central nervous system. By modulating neuroinflammation and synaptic function, oxysterols provide a mechanistic link between metabolic dysfunction and cognitive decline.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Oxysterols/metabolism
Animals
*Gastrointestinal Microbiome/physiology
*Brain/metabolism
Homeostasis/physiology
*Liver/metabolism
Signal Transduction/physiology
*Neurodegenerative Diseases/metabolism
RevDate: 2026-05-25
Chitosan-Loaded Melatonin Carbon Dots-Copper Nanocomposite Improves Rice Seedling Salt Tolerance via Scavenging-Regulation-Repair Trilevel Synergistic Mechanisms.
Journal of agricultural and food chemistry [Epub ahead of print].
Soil salinity severely limits rice growth, necessitating effective and safe mitigation strategies. Here, a chitosan-encapsulated melatonin carbon dots-copper nanocomposite (MT-CDs@Cs-Cu) was developed to enhance rice salt tolerance via a trilevel "scavenging-regulation-repair" mechanism. The nanocomposite effectively scavenges reactive oxygen and nitrogen species, activates antioxidant enzymes, and reduces oxidative damage. It suppresses ABA accumulation while upregulating aquaporin genes, improving stomatal conductance and water transport. Under salt stress, MT-CDs@Cs-Cu increases the germination rate, fresh weight, and chlorophyll content, while reducing Na[+] accumulation and elevating the K[+]/Na[+] ratio. Furthermore, it reconstructs the rhizosphere microbiome, enriching beneficial taxa such as Sphingomonas and Actinobacteria, and reverses salt-induced metabolic disturbances. This integrated strategy provides an effective framework for developing nanoagricultural technologies to mitigate soil salinization and enhance sustainable crop production.
Additional Links: PMID-42178903
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PubMed:
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@article {pmid42178903,
year = {2026},
author = {Xu, M and Peng, S and Sun, T and Liang, H and Hu, Q and Feng, G and Luo, J and Tan, L and Zhang, J and Fang, J},
title = {Chitosan-Loaded Melatonin Carbon Dots-Copper Nanocomposite Improves Rice Seedling Salt Tolerance via Scavenging-Regulation-Repair Trilevel Synergistic Mechanisms.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c11334},
pmid = {42178903},
issn = {1520-5118},
abstract = {Soil salinity severely limits rice growth, necessitating effective and safe mitigation strategies. Here, a chitosan-encapsulated melatonin carbon dots-copper nanocomposite (MT-CDs@Cs-Cu) was developed to enhance rice salt tolerance via a trilevel "scavenging-regulation-repair" mechanism. The nanocomposite effectively scavenges reactive oxygen and nitrogen species, activates antioxidant enzymes, and reduces oxidative damage. It suppresses ABA accumulation while upregulating aquaporin genes, improving stomatal conductance and water transport. Under salt stress, MT-CDs@Cs-Cu increases the germination rate, fresh weight, and chlorophyll content, while reducing Na[+] accumulation and elevating the K[+]/Na[+] ratio. Furthermore, it reconstructs the rhizosphere microbiome, enriching beneficial taxa such as Sphingomonas and Actinobacteria, and reverses salt-induced metabolic disturbances. This integrated strategy provides an effective framework for developing nanoagricultural technologies to mitigate soil salinization and enhance sustainable crop production.},
}
RevDate: 2026-05-25
Proton pump inhibitors in acute-on-chronic liver failure: a sheep in a sheep's clothing.
Revista espanola de enfermedades digestivas [Epub ahead of print].
Proton pump inhibitors (PPIs) are one of the safest drugs available which are largely overprescribed in clinical practice. Preclinical studies have suggested that chronic use of PPIs may alter gut microbiome and could promote gastrointestinal infections. Although the number-to-treat for a single infection event is high, the risk in patients with end-stage liver disease could be increased due to inherent immune-suppression, altered gastroenteric barrier and opportunity for bacterial translocation resulting in spontaneous bacterial peritonitis. In the present issue of the Spanish Journal of Gastroenterology, García Gavilán et al. published a prospective multicenter Andalusian study including 59 patients with acute-on-chronic liver failure (ACLF), among whom 26 patients were chronically exposed to PPI. Patients with and without PPIs showed a comparable grade of ACLF, rate of complications, and mortality. The rates of infection and length of hospitalization were also evenly distributed in patients exposed and not exposed to PPIs. These results add to the existing evidence and discourage deprescription of PPIs in patients with ACLF if otherwise indicated.
Additional Links: PMID-42179053
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PubMed:
Citation:
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@article {pmid42179053,
year = {2026},
author = {Rodríguez-Perálvarez, ML},
title = {Proton pump inhibitors in acute-on-chronic liver failure: a sheep in a sheep's clothing.},
journal = {Revista espanola de enfermedades digestivas},
volume = {},
number = {},
pages = {},
doi = {10.17235/reed.2026.12005/2026},
pmid = {42179053},
issn = {1130-0108},
abstract = {Proton pump inhibitors (PPIs) are one of the safest drugs available which are largely overprescribed in clinical practice. Preclinical studies have suggested that chronic use of PPIs may alter gut microbiome and could promote gastrointestinal infections. Although the number-to-treat for a single infection event is high, the risk in patients with end-stage liver disease could be increased due to inherent immune-suppression, altered gastroenteric barrier and opportunity for bacterial translocation resulting in spontaneous bacterial peritonitis. In the present issue of the Spanish Journal of Gastroenterology, García Gavilán et al. published a prospective multicenter Andalusian study including 59 patients with acute-on-chronic liver failure (ACLF), among whom 26 patients were chronically exposed to PPI. Patients with and without PPIs showed a comparable grade of ACLF, rate of complications, and mortality. The rates of infection and length of hospitalization were also evenly distributed in patients exposed and not exposed to PPIs. These results add to the existing evidence and discourage deprescription of PPIs in patients with ACLF if otherwise indicated.},
}
RevDate: 2026-05-25
CmpDate: 2026-05-25
The microbiome-gerogene axis: a new frontier in precision geromedicine.
Frontiers in aging, 7:1794192.
Aging is increasingly recognized as a biologically heterogeneous process arising from dynamic interactions among genetic programs, environmental exposures, and adaptive physiological responses. Within the geroscience framework, conserved hallmarks, including genomic instability, epigenetic alterations, mitochondrial dysfunction, chronic inflammation, cellular senescence, and dysbiosis, capture the systems-level nature of age-related decline. Parallel to this framework, the concept of gerogenes defines coordinated molecular programs that actively drive biological aging when persistently engaged, counterbalanced by gerosuppressive pathways that preserve resilience. Here, we synthesize evidence supporting a unifying microbiome-gerogene axis in which the gut microbiome functions as an upstream, modifiable regulator of molecular aging trajectories. Age-associated microbial remodeling leads to loss of beneficial metabolic functions, including short-chain fatty acid production, bile acid transformation, and mitochondrial-supportive co-metabolism, with downstream effects on epithelial barrier integrity, immune homeostasis, and tissue repair. Integrated multi-omics studies link these microbial changes to host transcriptional, epigenomic, proteomic, and metabolomic signatures of biological aging, enabling mechanistic insights beyond taxonomic associations. Immune aging represents a major convergence point of microbiome-gerogene crosstalk, as dysbiosis driven barrier dysfunction and microbial translocation reinforce inflammaging, immunosenescence, and senescence-associated signaling networks. In parallel, microbial metabolites interface with epigenetic regulation, mitochondrial quality control, circadian biology, and gut-brain-immune communication, extending microbial influence to systemic and neurodegenerative aging processes. Building on this mechanistic foundation, we propose the microbiome-gerogene axis as an integrative framework for precision geromedicine, linking lifestyle exposures to intracellular aging programs and informing biomarker discovery and personalized interventions aimed at extending healthspan rather than treating late-stage disease.
Additional Links: PMID-42179443
PubMed:
Citation:
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@article {pmid42179443,
year = {2026},
author = {Bautista, J and López-Cortés, A},
title = {The microbiome-gerogene axis: a new frontier in precision geromedicine.},
journal = {Frontiers in aging},
volume = {7},
number = {},
pages = {1794192},
pmid = {42179443},
issn = {2673-6217},
abstract = {Aging is increasingly recognized as a biologically heterogeneous process arising from dynamic interactions among genetic programs, environmental exposures, and adaptive physiological responses. Within the geroscience framework, conserved hallmarks, including genomic instability, epigenetic alterations, mitochondrial dysfunction, chronic inflammation, cellular senescence, and dysbiosis, capture the systems-level nature of age-related decline. Parallel to this framework, the concept of gerogenes defines coordinated molecular programs that actively drive biological aging when persistently engaged, counterbalanced by gerosuppressive pathways that preserve resilience. Here, we synthesize evidence supporting a unifying microbiome-gerogene axis in which the gut microbiome functions as an upstream, modifiable regulator of molecular aging trajectories. Age-associated microbial remodeling leads to loss of beneficial metabolic functions, including short-chain fatty acid production, bile acid transformation, and mitochondrial-supportive co-metabolism, with downstream effects on epithelial barrier integrity, immune homeostasis, and tissue repair. Integrated multi-omics studies link these microbial changes to host transcriptional, epigenomic, proteomic, and metabolomic signatures of biological aging, enabling mechanistic insights beyond taxonomic associations. Immune aging represents a major convergence point of microbiome-gerogene crosstalk, as dysbiosis driven barrier dysfunction and microbial translocation reinforce inflammaging, immunosenescence, and senescence-associated signaling networks. In parallel, microbial metabolites interface with epigenetic regulation, mitochondrial quality control, circadian biology, and gut-brain-immune communication, extending microbial influence to systemic and neurodegenerative aging processes. Building on this mechanistic foundation, we propose the microbiome-gerogene axis as an integrative framework for precision geromedicine, linking lifestyle exposures to intracellular aging programs and informing biomarker discovery and personalized interventions aimed at extending healthspan rather than treating late-stage disease.},
}
RevDate: 2026-05-22
Author Correction: Acarbose redirects gut microbiome utilization of dietary carbohydrates to suppress anaphylaxis in mice.
Additional Links: PMID-42168567
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@article {pmid42168567,
year = {2026},
author = {Yakabe, K and Inoue, Y and Yanagisawa, Y and Imai, S and Suwa, S and Ando, M and Wu, Y and Kurokawa, R and Srirat, T and Haneda, T and Miki, T and Ito, M and Hirayama, A and Kurashima, Y and Fukuda, S and Hase, K and Suda, W and Takeyama, H and Hori, S and Kim, YG},
title = {Author Correction: Acarbose redirects gut microbiome utilization of dietary carbohydrates to suppress anaphylaxis in mice.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41564-026-02393-5},
pmid = {42168567},
issn = {2058-5276},
}
RevDate: 2026-05-21
Oral squamous cell carcinoma is associated with altered salivary microbiome structure and reduced community evenness.
Scientific reports pii:10.1038/s41598-026-54192-x [Epub ahead of print].
Oral squamous cell carcinoma (OSCC) remains a major global health burden, highlighting the need for improved non-invasive tools for early detection and disease monitoring. Because saliva is easily accessible and reflects the oral microenvironment, the salivary microbiome has emerged as a promising source of candidate biomarkers. In this study, we characterized the salivary microbiota of 113 individuals, including 52 patients with OSCC and 61 healthy controls, using 16S rRNA gene sequencing targeting the V3-V4 region. Microbial diversity and composition were analyzed using complementary bioinformatic and statistical approaches, including four differential abundance methods (MaAsLin2, ANCOM-BC2, LinDA, and ALDEx2). OSCC was associated with significant differences in overall microbial community structure, as shown by beta diversity analyses, together with reduced community evenness but no major loss of richness. Differential abundance analyses identified several taxa overrepresented in OSCC, including the genera Tannerella, Solobacterium, Dialister, and Bergeyella, as well as species such as Solobacterium moorei, Tannerella forsythia, and Prevotella nigrescens. In contrast, Leptotrichia was underrepresented in OSCC. These findings support the existence of an OSCC-associated salivary dysbiosis characterized by ecological restructuring rather than global diversity loss. The identified taxa represent exploratory candidate microbial signatures associated with OSCC that require validation in larger, independent, and longitudinal cohorts before any potential clinical application can be considered.
Additional Links: PMID-42168582
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PubMed:
Citation:
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@article {pmid42168582,
year = {2026},
author = {Ferriz-Jordán, M and Hervás, D and Bagan, L and Gimeno, C and Herreros-Pomares, A and Bagán, J},
title = {Oral squamous cell carcinoma is associated with altered salivary microbiome structure and reduced community evenness.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-54192-x},
pmid = {42168582},
issn = {2045-2322},
support = {PID2022-138398OB-I00//Ministerio de Ciencia e Innovación/ ; },
abstract = {Oral squamous cell carcinoma (OSCC) remains a major global health burden, highlighting the need for improved non-invasive tools for early detection and disease monitoring. Because saliva is easily accessible and reflects the oral microenvironment, the salivary microbiome has emerged as a promising source of candidate biomarkers. In this study, we characterized the salivary microbiota of 113 individuals, including 52 patients with OSCC and 61 healthy controls, using 16S rRNA gene sequencing targeting the V3-V4 region. Microbial diversity and composition were analyzed using complementary bioinformatic and statistical approaches, including four differential abundance methods (MaAsLin2, ANCOM-BC2, LinDA, and ALDEx2). OSCC was associated with significant differences in overall microbial community structure, as shown by beta diversity analyses, together with reduced community evenness but no major loss of richness. Differential abundance analyses identified several taxa overrepresented in OSCC, including the genera Tannerella, Solobacterium, Dialister, and Bergeyella, as well as species such as Solobacterium moorei, Tannerella forsythia, and Prevotella nigrescens. In contrast, Leptotrichia was underrepresented in OSCC. These findings support the existence of an OSCC-associated salivary dysbiosis characterized by ecological restructuring rather than global diversity loss. The identified taxa represent exploratory candidate microbial signatures associated with OSCC that require validation in larger, independent, and longitudinal cohorts before any potential clinical application can be considered.},
}
RevDate: 2026-05-21
Skin aging: mechanisms, evaluation, and rejuvenation.
The EMBO journal [Epub ahead of print].
Skin aging, the most visible and accessible manifestation of organismal aging, reflects systemic physiological decline, compromising barrier integrity, immune defense, and regenerative capacity-functions essential for overall tissue homeostasis and longevity. Understanding why and how the skin ages offers crucial insights into tissue homeostasis and systemic aging. Here, we dissect the multi-layered mechanisms of skin aging across the epidermis, dermis, and appendages, highlighting how intrinsic cellular senescence, disrupted inter-compartmental communication, and dysregulation of the skin microbiome and hormonal signaling collectively undermine epithelial structure and function. We also summarize advances in quantitative evaluation of skin aging, from molecular signatures to morphological, microbial, and phenotypic indices, enabling objective assessment of biological age and intervention efficacy. Finally, we highlight rejuvenation strategies, encompassing rewiring of gene expression programs, metabolic modulation, microenvironmental remodeling, microbiome modulation, and hormone regulation, offering a framework for precision interventions and next-generation regenerative therapies.
Additional Links: PMID-42168603
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Citation:
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@article {pmid42168603,
year = {2026},
author = {Li, R and Zhang, J and Mao, K and Meng, D and Han, JJ},
title = {Skin aging: mechanisms, evaluation, and rejuvenation.},
journal = {The EMBO journal},
volume = {},
number = {},
pages = {},
pmid = {42168603},
issn = {1460-2075},
support = {32088101//MOST | National Natural Science Foundation of China (NSFC)/ ; 92374207//MOST | National Natural Science Foundation of China (NSFC)/ ; 32330017//MOST | National Natural Science Foundation of China (NSFC)/ ; 82361148130//MOST | National Natural Science Foundation of China (NSFC)/ ; 92049302//MOST | National Natural Science Foundation of China (NSFC)/ ; IS23077//| Natural Science Foundation of Beijing Municipality ()/ ; L254002//| Natural Science Foundation of Beijing Municipality ()/ ; 2020YFA0804000//Ministry of Science and Technology of the People's Republic of China (MOST)/ ; },
abstract = {Skin aging, the most visible and accessible manifestation of organismal aging, reflects systemic physiological decline, compromising barrier integrity, immune defense, and regenerative capacity-functions essential for overall tissue homeostasis and longevity. Understanding why and how the skin ages offers crucial insights into tissue homeostasis and systemic aging. Here, we dissect the multi-layered mechanisms of skin aging across the epidermis, dermis, and appendages, highlighting how intrinsic cellular senescence, disrupted inter-compartmental communication, and dysregulation of the skin microbiome and hormonal signaling collectively undermine epithelial structure and function. We also summarize advances in quantitative evaluation of skin aging, from molecular signatures to morphological, microbial, and phenotypic indices, enabling objective assessment of biological age and intervention efficacy. Finally, we highlight rejuvenation strategies, encompassing rewiring of gene expression programs, metabolic modulation, microenvironmental remodeling, microbiome modulation, and hormone regulation, offering a framework for precision interventions and next-generation regenerative therapies.},
}
RevDate: 2026-05-21
The Gut-Liver Axis in Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): Mechanisms, Microbiome Interactions and Therapeutic Targets.
Probiotics and antimicrobial proteins [Epub ahead of print].
Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a multifactorial condition in which the gut-liver axis plays a central pathogenic role. While a large body of literature has described associations between gut microbiota alterations and MASLD, a critical synthesis of the mechanistic pathways linking microbial activity to liver injury remains lacking. This review specifically focuses on gut-derived microbial metabolites as key mediators of disease progression. We examine how short-chain fatty acids, bile acids, lipopolysaccharide (LPS), trimethylamine-N-oxide (TMAO) and microbially derived ethanol influence hepatic lipid metabolism, inflammation and fibrogenesis through defined molecular pathways, including FXR signaling, TLR4 activation and immune-metabolic crosstalk. Importantly, we highlight inconsistencies in human microbiome studies, limitations in establishing causality and the challenges in translating preclinical findings into effective therapies. Although microbiome-targeted interventions such as probiotics, bile acid modulators and fecal microbiota transplantation show promise, their clinical efficacy remains variable due to interindividual heterogeneity and lack of mechanistic precision.By integrating current mechanistic evidence with translational insights, this review identifies critical knowledge gaps and proposes future directions for metabolite-focused therapeutic strategies. A more precise understanding of gut-derived signaling pathways will be essential to move from associative microbiome research toward targeted and personalized interventions in MASLD.
Additional Links: PMID-42168694
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Citation:
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@article {pmid42168694,
year = {2026},
author = {Sahu, P and Satapathy, T},
title = {The Gut-Liver Axis in Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): Mechanisms, Microbiome Interactions and Therapeutic Targets.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {42168694},
issn = {1867-1314},
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a multifactorial condition in which the gut-liver axis plays a central pathogenic role. While a large body of literature has described associations between gut microbiota alterations and MASLD, a critical synthesis of the mechanistic pathways linking microbial activity to liver injury remains lacking. This review specifically focuses on gut-derived microbial metabolites as key mediators of disease progression. We examine how short-chain fatty acids, bile acids, lipopolysaccharide (LPS), trimethylamine-N-oxide (TMAO) and microbially derived ethanol influence hepatic lipid metabolism, inflammation and fibrogenesis through defined molecular pathways, including FXR signaling, TLR4 activation and immune-metabolic crosstalk. Importantly, we highlight inconsistencies in human microbiome studies, limitations in establishing causality and the challenges in translating preclinical findings into effective therapies. Although microbiome-targeted interventions such as probiotics, bile acid modulators and fecal microbiota transplantation show promise, their clinical efficacy remains variable due to interindividual heterogeneity and lack of mechanistic precision.By integrating current mechanistic evidence with translational insights, this review identifies critical knowledge gaps and proposes future directions for metabolite-focused therapeutic strategies. A more precise understanding of gut-derived signaling pathways will be essential to move from associative microbiome research toward targeted and personalized interventions in MASLD.},
}
RevDate: 2026-05-24
CmpDate: 2026-05-21
Meta-analytic microbiome target discovery for immune checkpoint inhibitor response in advanced melanoma.
Communications medicine, 6(1):.
BACKGROUND: Immune checkpoint inhibitors have transformed melanoma therapy, yet only a subset of patients achieve durable responses. Gut microbes have been linked to response, but reported biomarkers vary across studies. We aim to identify reproducible microbial features and test their generalizability across cohorts and treatment settings.
METHODS: We reprocessed stool metagenomic sequencing data from 15 melanoma cohorts (763 samples from 484 individuals), including 12 cohorts treated with immune checkpoint inhibitors alone and 3 trials combining immune checkpoint inhibitors with fecal microbiota transplantation. Using a unified analysis pipeline, we profiled microbial species, metabolic pathways, and biosynthetic gene clusters, and analyzed their associations with treatment response using Tweedie regression, random-effects meta-analysis, and multimodal integration with leave-one-dataset-out validation.
RESULTS: Here, we show that responders in immune checkpoint inhibitor-only cohorts are enriched for several short-chain fatty acid-producing commensals, whereas non-responders show higher abundance of taxa associated with disrupted gut communities. In fecal microbiota transplantation plus immune checkpoint inhibitor trials, response associates with distinct communities and shifts in amino-acid, nucleotide and cofactor metabolism. Across cohorts, multiview prediction models repeatedly select gene clusters linked to antimicrobial peptides and surface polysaccharides, but cross-study discrimination remains modest.
CONCLUSIONS: Microbiome signatures of response are treatment-context dependent and are not captured by a single universal species. These harmonized findings prioritize microbial taxa and functions for mechanistic studies and future microbiome-informed interventions.
Additional Links: PMID-42168704
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Citation:
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@article {pmid42168704,
year = {2026},
author = {Zhang, X and Mallick, H and Rahnavard, A},
title = {Meta-analytic microbiome target discovery for immune checkpoint inhibitor response in advanced melanoma.},
journal = {Communications medicine},
volume = {6},
number = {1},
pages = {},
pmid = {42168704},
issn = {2730-664X},
support = {2109688//National Science Foundation (NSF)/ ; 2109688//National Science Foundation (NSF)/ ; },
abstract = {BACKGROUND: Immune checkpoint inhibitors have transformed melanoma therapy, yet only a subset of patients achieve durable responses. Gut microbes have been linked to response, but reported biomarkers vary across studies. We aim to identify reproducible microbial features and test their generalizability across cohorts and treatment settings.
METHODS: We reprocessed stool metagenomic sequencing data from 15 melanoma cohorts (763 samples from 484 individuals), including 12 cohorts treated with immune checkpoint inhibitors alone and 3 trials combining immune checkpoint inhibitors with fecal microbiota transplantation. Using a unified analysis pipeline, we profiled microbial species, metabolic pathways, and biosynthetic gene clusters, and analyzed their associations with treatment response using Tweedie regression, random-effects meta-analysis, and multimodal integration with leave-one-dataset-out validation.
RESULTS: Here, we show that responders in immune checkpoint inhibitor-only cohorts are enriched for several short-chain fatty acid-producing commensals, whereas non-responders show higher abundance of taxa associated with disrupted gut communities. In fecal microbiota transplantation plus immune checkpoint inhibitor trials, response associates with distinct communities and shifts in amino-acid, nucleotide and cofactor metabolism. Across cohorts, multiview prediction models repeatedly select gene clusters linked to antimicrobial peptides and surface polysaccharides, but cross-study discrimination remains modest.
CONCLUSIONS: Microbiome signatures of response are treatment-context dependent and are not captured by a single universal species. These harmonized findings prioritize microbial taxa and functions for mechanistic studies and future microbiome-informed interventions.},
}
RevDate: 2026-05-21
A new sparse Bayesian quantile neural network-based approach and its application to discover physiological sweet spots in the Canadian Longitudinal Study on Aging.
GeroScience [Epub ahead of print].
Identifying physiological sweet spots (optimal ranges for homeostasis) is essential for precision medicine. However, traditional statistical methods often rely on globally linear or locally jagged models that struggle to capture the smooth, non-linear nature of biological regulation in high-dimensional data. We present the Quantile Feature Selection Network (Q‑FSNet), a neural network-based framework that integrates quantile regression, feature selection, and uncertainty estimation to identify biomarkers with sweet spots. Unlike traditional methods, Q-FSNet learns continuous response curves without requiring a pre-specified number of change points. We further introduce Quantile Dirichlet Network (Q-DirichNet), a fully Bayesian extension that utilizes Dirichlet priors to automate feature shrinkage. Using data from the Canadian Longitudinal Study on Aging, we identified 25 metabolites with distinct homeostatic ranges for which biological age acceleration is minimized. The metabolites with sweet spots for biological aging include some derived from diet or produced by the gut microbiome; this highlights their potential for knowledge translation and public health impact. Our results, corroborated by existing literature, demonstrate that these sparse neural network-based methods offer a scalable and interpretable tool for discovering metabolic signatures of healthy aging vs. dysregulation in large-scale omics research.
Additional Links: PMID-42168723
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Citation:
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@article {pmid42168723,
year = {2026},
author = {Min, J and Vishnyakova, O and Brooks-Wilson, A and Elliott, LT},
title = {A new sparse Bayesian quantile neural network-based approach and its application to discover physiological sweet spots in the Canadian Longitudinal Study on Aging.},
journal = {GeroScience},
volume = {},
number = {},
pages = {},
pmid = {42168723},
issn = {2509-2723},
support = {PAD 179760/CAPMC/CIHR/Canada ; },
abstract = {Identifying physiological sweet spots (optimal ranges for homeostasis) is essential for precision medicine. However, traditional statistical methods often rely on globally linear or locally jagged models that struggle to capture the smooth, non-linear nature of biological regulation in high-dimensional data. We present the Quantile Feature Selection Network (Q‑FSNet), a neural network-based framework that integrates quantile regression, feature selection, and uncertainty estimation to identify biomarkers with sweet spots. Unlike traditional methods, Q-FSNet learns continuous response curves without requiring a pre-specified number of change points. We further introduce Quantile Dirichlet Network (Q-DirichNet), a fully Bayesian extension that utilizes Dirichlet priors to automate feature shrinkage. Using data from the Canadian Longitudinal Study on Aging, we identified 25 metabolites with distinct homeostatic ranges for which biological age acceleration is minimized. The metabolites with sweet spots for biological aging include some derived from diet or produced by the gut microbiome; this highlights their potential for knowledge translation and public health impact. Our results, corroborated by existing literature, demonstrate that these sparse neural network-based methods offer a scalable and interpretable tool for discovering metabolic signatures of healthy aging vs. dysregulation in large-scale omics research.},
}
RevDate: 2026-05-21
Impact of an online-guided physical activity intervention on cognition, resting-state brain connectivity, and the gut microbiome in healthy older adults-a randomized controlled trial.
GeroScience [Epub ahead of print].
INTRODUCTION: Physical activity may enhance cognition in older adults, yet evidence from randomized controlled trials (RCTs) on mechanistic pathways remains inconclusive.
METHODS: This single-blinded RCT examined the effects of an 8-week, online-guided, multicomponent physical activity intervention on cognitive function, resting-state functional brain connectivity (rsFC), and the gut microbiome in 92 healthy older adults (M age = 66.35). Participants were randomized to a physical activity group performing moderate-to-vigorous-intensity aerobic, coordination, and balance exercises, or to an active control group engaging in progressive muscle relaxation and listening to aging-related podcasts. The primary outcome was change in visual processing speed (items/s) from pre- to post-assessment. Secondary outcomes included changes in additional cognitive measures, rsFC, cardiorespiratory fitness (CRF), and the gut microbiome.
RESULTS: The primary outcome showed no significant between-group differences. However, exploratory analyses revealed potential improvements in inhibition (η2 = 0.061; p = 0.025) and visual memory (η2 = 0.047; p = 0.040) in the physical activity group. This group also showed a potential increase in rsFC between visual and dorsal attention networks (η2 = 0.101; p = 0.009). Visual memory gains correlated with improvements in rsFC (p = 0.013). No between-group differences were observed in CRF or gut microbiome composition.
DISCUSSION: While the primary outcome (visual processing speed) and predefined mechanistic pathways (e.g., gut microbiome composition) remained unaffected, this may partly reflect the sample's high baseline fitness, which likely limited observable improvements. Exploratory findings suggest potential cognitive and associated rsFC benefits in memory and attention-related networks. The online format enabled a structured, scalable intervention while minimizing potential confounding from social interaction.
TRIAL REGISTRATION: https://drks.de/search/de/trial/DRKS00028022 (date of registration: 14.02.2022).
Additional Links: PMID-42168724
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Citation:
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@article {pmid42168724,
year = {2026},
author = {Schrenk, SJ and Bang, C and Best, L and Dost, T and Flor, S and Frahm, C and Gaser, C and Hamdan, RA and Herbsleb, M and Kaleta, C and Kattlun, F and Müller, HJ and Puta, C and Radscheidt, M and Ruiz-Rizzo, AL and Scherag, A and Steidten, T and Witte, OW and Brodoehl, S and Finke, K},
title = {Impact of an online-guided physical activity intervention on cognition, resting-state brain connectivity, and the gut microbiome in healthy older adults-a randomized controlled trial.},
journal = {GeroScience},
volume = {},
number = {},
pages = {},
pmid = {42168724},
issn = {2509-2723},
support = {859890//Horizon 2020 Framework Programme/ ; FI 1424/2-2//Deutsche Forschungsgemeinschaft/ ; P2019-01-006//Carl-Zeiss-Stiftung/ ; },
abstract = {INTRODUCTION: Physical activity may enhance cognition in older adults, yet evidence from randomized controlled trials (RCTs) on mechanistic pathways remains inconclusive.
METHODS: This single-blinded RCT examined the effects of an 8-week, online-guided, multicomponent physical activity intervention on cognitive function, resting-state functional brain connectivity (rsFC), and the gut microbiome in 92 healthy older adults (M age = 66.35). Participants were randomized to a physical activity group performing moderate-to-vigorous-intensity aerobic, coordination, and balance exercises, or to an active control group engaging in progressive muscle relaxation and listening to aging-related podcasts. The primary outcome was change in visual processing speed (items/s) from pre- to post-assessment. Secondary outcomes included changes in additional cognitive measures, rsFC, cardiorespiratory fitness (CRF), and the gut microbiome.
RESULTS: The primary outcome showed no significant between-group differences. However, exploratory analyses revealed potential improvements in inhibition (η2 = 0.061; p = 0.025) and visual memory (η2 = 0.047; p = 0.040) in the physical activity group. This group also showed a potential increase in rsFC between visual and dorsal attention networks (η2 = 0.101; p = 0.009). Visual memory gains correlated with improvements in rsFC (p = 0.013). No between-group differences were observed in CRF or gut microbiome composition.
DISCUSSION: While the primary outcome (visual processing speed) and predefined mechanistic pathways (e.g., gut microbiome composition) remained unaffected, this may partly reflect the sample's high baseline fitness, which likely limited observable improvements. Exploratory findings suggest potential cognitive and associated rsFC benefits in memory and attention-related networks. The online format enabled a structured, scalable intervention while minimizing potential confounding from social interaction.
TRIAL REGISTRATION: https://drks.de/search/de/trial/DRKS00028022 (date of registration: 14.02.2022).},
}
RevDate: 2026-05-22
Exploring microbial ecology in public swimming pools: a metagenomic investigation of community structure and environmental correlates.
BMC microbiology pii:10.1186/s12866-026-05157-7 [Epub ahead of print].
Epidemiological studies have identified correlations between swimming and outbreaks of various infectious diseases. However, a comprehensive understanding of the pathogens present in public swimming pool water has yet to be systematically established. Swimming pool water samples were collected from 20 indoor public swimming pools in Shanghai, China during the summer of 2023. After quality inspection of the extracted nucleic acid, the qualified samples were subjected to metagenomic sequencing to profile the microbial communities of swimming pool water. A total of 24,035 microbial species were identified with the abundance of bacteria (99.46%), followed by archaea (0.29%), viruses (0.20%), and fungi (0.05%), including 441 pathogenic species, 23 of which were classified as biosafety level 3 (BSL-3) microorganisms. Environmental sources constituted the dominant origin (86.00%) of the pool water microbiome. Additionally, suburban pools demonstrated greater microbial diversity than urban pools (P < 0.05). The abundance of viruses exhibited a positive correlation with the concentration of urea in pool water (r = 0.31, P < 0.05). This study demonstrated that swimming pool water serves as a potent reservoir and mixing vessel for various highly pathogenic microorganisms. Effective water quality management strategies are essential to mitigating the potential public health threats of public swimming pools.
Additional Links: PMID-42168837
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@article {pmid42168837,
year = {2026},
author = {Tong, L and Liu, Y and Han, F and Jiang, Y and Ying, S and Zhang, B and Cheng, Y and Liu, Z and Shi, Y and Xu, M and Tang, C and Sui, S and Chen, T},
title = {Exploring microbial ecology in public swimming pools: a metagenomic investigation of community structure and environmental correlates.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05157-7},
pmid = {42168837},
issn = {1471-2180},
support = {GWVI-4//The Key Projects in the Three-year Plan of Shanghai Municipal Public Health System (2023-2025)/ ; },
abstract = {Epidemiological studies have identified correlations between swimming and outbreaks of various infectious diseases. However, a comprehensive understanding of the pathogens present in public swimming pool water has yet to be systematically established. Swimming pool water samples were collected from 20 indoor public swimming pools in Shanghai, China during the summer of 2023. After quality inspection of the extracted nucleic acid, the qualified samples were subjected to metagenomic sequencing to profile the microbial communities of swimming pool water. A total of 24,035 microbial species were identified with the abundance of bacteria (99.46%), followed by archaea (0.29%), viruses (0.20%), and fungi (0.05%), including 441 pathogenic species, 23 of which were classified as biosafety level 3 (BSL-3) microorganisms. Environmental sources constituted the dominant origin (86.00%) of the pool water microbiome. Additionally, suburban pools demonstrated greater microbial diversity than urban pools (P < 0.05). The abundance of viruses exhibited a positive correlation with the concentration of urea in pool water (r = 0.31, P < 0.05). This study demonstrated that swimming pool water serves as a potent reservoir and mixing vessel for various highly pathogenic microorganisms. Effective water quality management strategies are essential to mitigating the potential public health threats of public swimming pools.},
}
RevDate: 2026-05-22
Integrative multi-omics analysis reveals host-microbiome metabolic alterations and candidate biomarkers in Parkinson's disease.
BMC microbiology pii:10.1186/s12866-026-05168-4 [Epub ahead of print].
Alterations in the gut microbiome have been increasingly implicated in Parkinson's disease (PD), but the associated metabolic changes remain incompletely understood. Here, we applied an integrative multi-omics approach combining shotgun metagenomic sequencing and untargeted LC-MS-based plasma metabolomics to investigate host-microbiome alterations in PD. Fecal and plasma samples were collected from 30 PD patients and 30 healthy spouse controls. Significant differences in microbial diversity and taxonomic composition were observed between the two groups. Taxonomic profiling revealed marked gut microbial dysbiosis in PD, including altered abundances of Phocea massiliensis, Bacteroides sp900766005, and Alistipes_A indistinctus. Metabolomic analysis identified 86 significantly altered plasma metabolites, including glycerophospholipids, indoleacetic acid, and kynurenic acid. Integrative pathway analysis suggested links between microbial functional alterations and host metabolic changes. Machine-learning analyses identified three biomarker panels that distinguished PD patients from controls in validation datasets, with the highest area under the curve (AUC) reaching 0.92. In silico molecular docking further suggested potential interactions between several metabolite biomarkers and alpha-2-macroglobulin (A2M) or the human B[act] spliceosome. Overall, these findings provide an integrative view of host-microbiome metabolic alterations associated with PD and highlight candidate biomarkers and exploratory host-metabolite associations for further investigation.
Additional Links: PMID-42168845
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@article {pmid42168845,
year = {2026},
author = {Zhao, Q and Zuo, S and Liu, S and Wang, J and Tang, J and Zou, X and Leng, Y and Li, X and Zhou, M and Tian, J and Wang, P},
title = {Integrative multi-omics analysis reveals host-microbiome metabolic alterations and candidate biomarkers in Parkinson's disease.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05168-4},
pmid = {42168845},
issn = {1471-2180},
support = {2023AFD045//Hubei Provincial Natural Science Foundation / Joint Fund Project Cultivation Project/ ; 2023BCB140//Hubei Provincial plan of science and technology key research project/ ; 2023XKQT1//The Advantages Dicipline Group (Medicine) Project in Higher Education of Hubei Province (2021-2025)/ ; },
abstract = {Alterations in the gut microbiome have been increasingly implicated in Parkinson's disease (PD), but the associated metabolic changes remain incompletely understood. Here, we applied an integrative multi-omics approach combining shotgun metagenomic sequencing and untargeted LC-MS-based plasma metabolomics to investigate host-microbiome alterations in PD. Fecal and plasma samples were collected from 30 PD patients and 30 healthy spouse controls. Significant differences in microbial diversity and taxonomic composition were observed between the two groups. Taxonomic profiling revealed marked gut microbial dysbiosis in PD, including altered abundances of Phocea massiliensis, Bacteroides sp900766005, and Alistipes_A indistinctus. Metabolomic analysis identified 86 significantly altered plasma metabolites, including glycerophospholipids, indoleacetic acid, and kynurenic acid. Integrative pathway analysis suggested links between microbial functional alterations and host metabolic changes. Machine-learning analyses identified three biomarker panels that distinguished PD patients from controls in validation datasets, with the highest area under the curve (AUC) reaching 0.92. In silico molecular docking further suggested potential interactions between several metabolite biomarkers and alpha-2-macroglobulin (A2M) or the human B[act] spliceosome. Overall, these findings provide an integrative view of host-microbiome metabolic alterations associated with PD and highlight candidate biomarkers and exploratory host-metabolite associations for further investigation.},
}
RevDate: 2026-05-22
Microbiota-Gut-Brain Axis in Neurodegenerative Diseases: The Role of Bacterial Amyloids.
Cellular and molecular gastroenterology and hepatology pii:S2352-345X(26)00080-9 [Epub ahead of print].
Neurodegenerative diseases are proteinopathies, characterized by misfolded protein aggregation in the brain that drives neuronal dysfunctions. Neurodegenerative diseases are also increasingly recognized as multi-organ disorders in which the gut plays a pivotal role. Indeed, recent advances in the research field of neurodegenerative diseases suggest that the gut is not merely a passive bystander, given the high prevalence of gastrointestinal symptoms, but a critical contributor to disease etiology, with evidence supporting a direct role in initiating and driving disease progression. Among environmental factors increasingly recognized as modulators of neurodegenerative disease progression, the gut microbiota has gained prominence. Beyond the impact of altered bacterial metabolites, growing evidence indicate a potential role of gut microbiota-derived amyloids in neurodegenerative diseases. For instance, gut microbial amyloids such as curli can cross-seed host proteins like α-synuclein and β-amyloid promoting aggregation, gut-to-brain propagation, and exacerbating neurodegeneration, revealing a novel mechanism linking the microbiome to neurodegenerative diseases. This conceptual shift opens promising avenues for strategies targeting the gut microbiota, including therapeutic and preventive interventions aimed at reshaping microbial communities or limiting exposure to pathogenic amyloids to reduce risk of neurodegenerative diseases. Here, we review recent discoveries to elucidate the complex interplay between gut microbiota and host amyloids, offering insights for enhancing gut and brain health and potentially preventing or reversing neurodegenerative disease progression.
Additional Links: PMID-42103282
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@article {pmid42103282,
year = {2026},
author = {Cissé, M and Moullé, V and Brossaud, R and Oullier, T and Neunlist, M},
title = {Microbiota-Gut-Brain Axis in Neurodegenerative Diseases: The Role of Bacterial Amyloids.},
journal = {Cellular and molecular gastroenterology and hepatology},
volume = {},
number = {},
pages = {101802},
doi = {10.1016/j.jcmgh.2026.101802},
pmid = {42103282},
issn = {2352-345X},
abstract = {Neurodegenerative diseases are proteinopathies, characterized by misfolded protein aggregation in the brain that drives neuronal dysfunctions. Neurodegenerative diseases are also increasingly recognized as multi-organ disorders in which the gut plays a pivotal role. Indeed, recent advances in the research field of neurodegenerative diseases suggest that the gut is not merely a passive bystander, given the high prevalence of gastrointestinal symptoms, but a critical contributor to disease etiology, with evidence supporting a direct role in initiating and driving disease progression. Among environmental factors increasingly recognized as modulators of neurodegenerative disease progression, the gut microbiota has gained prominence. Beyond the impact of altered bacterial metabolites, growing evidence indicate a potential role of gut microbiota-derived amyloids in neurodegenerative diseases. For instance, gut microbial amyloids such as curli can cross-seed host proteins like α-synuclein and β-amyloid promoting aggregation, gut-to-brain propagation, and exacerbating neurodegeneration, revealing a novel mechanism linking the microbiome to neurodegenerative diseases. This conceptual shift opens promising avenues for strategies targeting the gut microbiota, including therapeutic and preventive interventions aimed at reshaping microbial communities or limiting exposure to pathogenic amyloids to reduce risk of neurodegenerative diseases. Here, we review recent discoveries to elucidate the complex interplay between gut microbiota and host amyloids, offering insights for enhancing gut and brain health and potentially preventing or reversing neurodegenerative disease progression.},
}
RevDate: 2026-05-21
CmpDate: 2026-05-21
Axillary and gut microbiota characteristics in axillary bromhidrosis patients and the effect of microwave therapy: a case-control study.
Frontiers in microbiology, 17:1769465.
INTRODUCTION: Axillary bromhidrosis is characterized by excessive sweat gland activity and foul body odor, significantly affecting patients' psychological well-being and social interactions.
METHODS: This study recruited 30 axillary bromhidrosis patients and 30 healthy controls, collecting sweat and stool samples for microbiome analysis. Among the patients, 8 patients received microwave therapy, collecting pre- and post-treatment samples for microbiome analysis.
RESULTS: The axillary microbiota of patients showed significant differences compared to healthy controls, particularly with increased abundance of odor-causing bacteria such as Staphylococcus and related species (Staphylococcus hominis, Staphylococcus haemolyticus) (LDA > 3, p < 0.05). While the gut microbiota composition showed no significant changes, but LEfSe analysis revealed that SCFAs-producing bacteria (Bacteroides stercoris, Phocaeicola massiliensis, and Phocaeicola vulgatus) was significantly elevated (LDA > 3, p < 0.05), indicating that the abundance changes of SCFAs-producing bacteria may be associated with axillary odor production through the regulation of metabolic processes. Correlation analysis revealed positive correlations between axillary odor-producing genera (Staphylococcus, Peptoniphilus, Anaerococcus) and gut SCFAs-producing genera (Roseburia, Blautia, Clostridium), suggesting a bidirectional microbiota network through gut-derived butyrate production and immune modulation (p < 0.05). However, further experimentals are required to confirm the causal relationship. Furthermore, microwave therapy significantly altered axillary microbiota diversity, potentially alleviating axillary odor by inhibiting odor-producing bacteria (Staphylococcus) (LDA > 3, p < 0.05), while exerting minimal impact on the gut microbiota. KEGG pathway enrichment analysis revealed significant metabolic activity changes in lipid, carbohydrate, sulfur, and amino acid metabolism pathways.
CONCLUSION: This study is the first to demonstrate the interrelationship between the axillary and gut microbiota in axillary bromhidrosis patients, showing a link between gut-derived butyrate production and axillary odor. These findings offer new insights into the microbiological mechanisms underlying axillary bromhidrosis and identify potential microbial targets for future gut-based systemic treatments.
Additional Links: PMID-42164666
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid42164666,
year = {2026},
author = {Wu, X and Li, M and Xu, Y and Liu, X and Gao, Z and Jiang, X and He, J and Wu, Y and Wu, C},
title = {Axillary and gut microbiota characteristics in axillary bromhidrosis patients and the effect of microwave therapy: a case-control study.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1769465},
pmid = {42164666},
issn = {1664-302X},
abstract = {INTRODUCTION: Axillary bromhidrosis is characterized by excessive sweat gland activity and foul body odor, significantly affecting patients' psychological well-being and social interactions.
METHODS: This study recruited 30 axillary bromhidrosis patients and 30 healthy controls, collecting sweat and stool samples for microbiome analysis. Among the patients, 8 patients received microwave therapy, collecting pre- and post-treatment samples for microbiome analysis.
RESULTS: The axillary microbiota of patients showed significant differences compared to healthy controls, particularly with increased abundance of odor-causing bacteria such as Staphylococcus and related species (Staphylococcus hominis, Staphylococcus haemolyticus) (LDA > 3, p < 0.05). While the gut microbiota composition showed no significant changes, but LEfSe analysis revealed that SCFAs-producing bacteria (Bacteroides stercoris, Phocaeicola massiliensis, and Phocaeicola vulgatus) was significantly elevated (LDA > 3, p < 0.05), indicating that the abundance changes of SCFAs-producing bacteria may be associated with axillary odor production through the regulation of metabolic processes. Correlation analysis revealed positive correlations between axillary odor-producing genera (Staphylococcus, Peptoniphilus, Anaerococcus) and gut SCFAs-producing genera (Roseburia, Blautia, Clostridium), suggesting a bidirectional microbiota network through gut-derived butyrate production and immune modulation (p < 0.05). However, further experimentals are required to confirm the causal relationship. Furthermore, microwave therapy significantly altered axillary microbiota diversity, potentially alleviating axillary odor by inhibiting odor-producing bacteria (Staphylococcus) (LDA > 3, p < 0.05), while exerting minimal impact on the gut microbiota. KEGG pathway enrichment analysis revealed significant metabolic activity changes in lipid, carbohydrate, sulfur, and amino acid metabolism pathways.
CONCLUSION: This study is the first to demonstrate the interrelationship between the axillary and gut microbiota in axillary bromhidrosis patients, showing a link between gut-derived butyrate production and axillary odor. These findings offer new insights into the microbiological mechanisms underlying axillary bromhidrosis and identify potential microbial targets for future gut-based systemic treatments.},
}
RevDate: 2026-05-21
CmpDate: 2026-05-21
Analysis of microbial diversity in Lagotis brevituba Maxim. from different production areas on the Qinghai-Xizang Plateau and its correlation with secondary metabolic products.
Frontiers in microbiology, 17:1797784.
Lagotis brevituba Maxim. (Lagotis brevituba), belonging to the genus Lagotis within the family Scrophulariaceae. The content of its secondary metabolites exhibits significant variation across different provenances, yet the underlying mechanisms linking these variations to microbial associations remain unclear. In this study, 12 samples of rhizosphere soil, root systems, and plant specimens of Lagotis brevituba were collected from various locations on the Qinghai-Xizang Plateau, and the physicochemical properties of the soil were systematically determined. Using high-throughput 16S and ITS rRNA sequencing technologies, the diversity and composition of bacterial and fungal communities were analyzed; simultaneously, the concentrations of 10 key secondary metabolites were quantitatively determined using high-performance liquid chromatography (HPLC). Furthermore, correlation network analysis and redundancy analysis were used to investigate the relationships among soil physicochemical factors, microbial communities, and secondary metabolites. The results indicate that an elevation of 4500 m serves as a critical threshold, marked by significant changes in soil physicochemical properties. Specifically, compared to the HA group (3500-4500 m), the EA group (elevation > 4500 m) exhibited significantly lower soil organic matter and available phosphorus content, while pH and total nitrogen content were significantly higher. These soil changes indicate the presence of nutrient-poor and alkaline stress conditions, which in turn led to the differentiation of rhizosphere bacterial communities and stimulated the synthesis of more antioxidant metabolites (e.g., significantly elevated β-Sitosterol, Quercetin, and Plantamajoside) in the EA group. Microbial community analysis revealed that bacterial community structure exhibited a significant response to changes in elevation, whereas fungal communities showed no significant differences. Soil physicochemical properties (particularly pH, SOM, and AP) are key mediating factors driving microbial community differentiation and the accumulation of secondary metabolites. A combined analysis of correlation networks and Zi-Pi values identified 19 key OTUs (Operational Taxonomic Units) mediating the relationships between microorganisms and metabolites. Notably, Aquabacterium exhibited significant negative correlations with Luteolin and Acteoside, while Streptomyces showed significant positive correlations with Hyperoside (P < 0.05). This study demonstrates that soil environmental factors structure microbial communities, which in turn play a crucial role in regulating the secondary metabolites of medicinal plants. These findings provide theoretical foundations for elucidating the environment-microbiome-metabolite nexus in Lagotis brevituba.
Additional Links: PMID-42164667
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid42164667,
year = {2026},
author = {Ma, H and Li, J and BanMa, C and Yuan, F and Chen, Y and Yang, X and Yang, X and Wang, T and Zhou, G},
title = {Analysis of microbial diversity in Lagotis brevituba Maxim. from different production areas on the Qinghai-Xizang Plateau and its correlation with secondary metabolic products.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1797784},
pmid = {42164667},
issn = {1664-302X},
abstract = {Lagotis brevituba Maxim. (Lagotis brevituba), belonging to the genus Lagotis within the family Scrophulariaceae. The content of its secondary metabolites exhibits significant variation across different provenances, yet the underlying mechanisms linking these variations to microbial associations remain unclear. In this study, 12 samples of rhizosphere soil, root systems, and plant specimens of Lagotis brevituba were collected from various locations on the Qinghai-Xizang Plateau, and the physicochemical properties of the soil were systematically determined. Using high-throughput 16S and ITS rRNA sequencing technologies, the diversity and composition of bacterial and fungal communities were analyzed; simultaneously, the concentrations of 10 key secondary metabolites were quantitatively determined using high-performance liquid chromatography (HPLC). Furthermore, correlation network analysis and redundancy analysis were used to investigate the relationships among soil physicochemical factors, microbial communities, and secondary metabolites. The results indicate that an elevation of 4500 m serves as a critical threshold, marked by significant changes in soil physicochemical properties. Specifically, compared to the HA group (3500-4500 m), the EA group (elevation > 4500 m) exhibited significantly lower soil organic matter and available phosphorus content, while pH and total nitrogen content were significantly higher. These soil changes indicate the presence of nutrient-poor and alkaline stress conditions, which in turn led to the differentiation of rhizosphere bacterial communities and stimulated the synthesis of more antioxidant metabolites (e.g., significantly elevated β-Sitosterol, Quercetin, and Plantamajoside) in the EA group. Microbial community analysis revealed that bacterial community structure exhibited a significant response to changes in elevation, whereas fungal communities showed no significant differences. Soil physicochemical properties (particularly pH, SOM, and AP) are key mediating factors driving microbial community differentiation and the accumulation of secondary metabolites. A combined analysis of correlation networks and Zi-Pi values identified 19 key OTUs (Operational Taxonomic Units) mediating the relationships between microorganisms and metabolites. Notably, Aquabacterium exhibited significant negative correlations with Luteolin and Acteoside, while Streptomyces showed significant positive correlations with Hyperoside (P < 0.05). This study demonstrates that soil environmental factors structure microbial communities, which in turn play a crucial role in regulating the secondary metabolites of medicinal plants. These findings provide theoretical foundations for elucidating the environment-microbiome-metabolite nexus in Lagotis brevituba.},
}
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