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ESP: PubMed Auto Bibliography 11 Mar 2026 at 01:55 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: 2026-03-09
Cuticle-associated microbiota in Bactrocera dorsalis suppress fungal infection through immune and chemical defenses.
Pest management science [Epub ahead of print].
BACKGROUND: Cuticular microbial communities influence insect-pathogen interactions, yet their protective roles remain incompletely understood. These microbial defenses are critical in pest species like Bactrocera dorsalis, where microbial symbionts may shape resistance to biological control agents.
RESULTS: We show that the cuticular microbiota of Bactrocera dorsalis enhances resistance to the entomopathogenic fungi (EPF) Beauveria bassiana and Isaria fumosorosea through dual immune and chemical mechanisms. Gnotobiotic assays demonstrate that specific bacterial isolates (Microbacterium, Psychrobacter, and Staphylococcus) promote host survival and defense by stimulating Toll/IMD signaling pathway and up-regulating antimicrobial peptides (AMPs) such as defensin, attacin, and cecropin. In contrast, non-cuticle-associated bacteria (Escherichia coli and Staphylococcus aureus) failed to enhance survival and immune responses, indicating that protection is microbiota-specific rather than a result of general bacterial exposure. In parallel, bacterial volatiles, such as phenol, indole, and eicosane, along with extracellular enzymes including chitinase, cellulase, protease, and lipase, suppressed fungal germination and hyphal growth. Importantly, these protective effects were found to vary with host age, indicating age-dependent modulation of microbiota-mediated defense.
CONCLUSIONS: Our findings revealed that cuticle-associated bacteria protect their host through complementary immune and chemical pathways. These microbiota act as an active barrier, and microbial metabolism interacts with host immune signaling. By distinguishing specific cuticle-derived effects from non-specific bacterial stimulation, this study highlighted the role of microbiota in modulating fungal susceptibility and supports their application in developing next-generation biocontrol strategies in pest management. © 2026 Society of Chemical Industry.
Additional Links: PMID-41800606
Publisher:
PubMed:
Citation:
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@article {pmid41800606,
year = {2026},
author = {Kabir, K and Afzal, I and Haider, K and Naiem, F and Li, X and Zhang, H},
title = {Cuticle-associated microbiota in Bactrocera dorsalis suppress fungal infection through immune and chemical defenses.},
journal = {Pest management science},
volume = {},
number = {},
pages = {},
doi = {10.1002/ps.70704},
pmid = {41800606},
issn = {1526-4998},
support = {//This study was supported by the National Natural Science Foundation of China (No. 32220103009), the China Agriculture Research System of MOF and MARA (CARS-26), and the Hubei Hongshan Laboratory./ ; },
abstract = {BACKGROUND: Cuticular microbial communities influence insect-pathogen interactions, yet their protective roles remain incompletely understood. These microbial defenses are critical in pest species like Bactrocera dorsalis, where microbial symbionts may shape resistance to biological control agents.
RESULTS: We show that the cuticular microbiota of Bactrocera dorsalis enhances resistance to the entomopathogenic fungi (EPF) Beauveria bassiana and Isaria fumosorosea through dual immune and chemical mechanisms. Gnotobiotic assays demonstrate that specific bacterial isolates (Microbacterium, Psychrobacter, and Staphylococcus) promote host survival and defense by stimulating Toll/IMD signaling pathway and up-regulating antimicrobial peptides (AMPs) such as defensin, attacin, and cecropin. In contrast, non-cuticle-associated bacteria (Escherichia coli and Staphylococcus aureus) failed to enhance survival and immune responses, indicating that protection is microbiota-specific rather than a result of general bacterial exposure. In parallel, bacterial volatiles, such as phenol, indole, and eicosane, along with extracellular enzymes including chitinase, cellulase, protease, and lipase, suppressed fungal germination and hyphal growth. Importantly, these protective effects were found to vary with host age, indicating age-dependent modulation of microbiota-mediated defense.
CONCLUSIONS: Our findings revealed that cuticle-associated bacteria protect their host through complementary immune and chemical pathways. These microbiota act as an active barrier, and microbial metabolism interacts with host immune signaling. By distinguishing specific cuticle-derived effects from non-specific bacterial stimulation, this study highlighted the role of microbiota in modulating fungal susceptibility and supports their application in developing next-generation biocontrol strategies in pest management. © 2026 Society of Chemical Industry.},
}
RevDate: 2026-03-09
Application of Artificial Intelligence-Powered Research in Gastrointestinal Pathophysiology: Unveiling Intestinal Pathobionts and Microbiota Dysbiosis.
Journal of physiological investigation [Epub ahead of print].
Additional Links: PMID-41800525
PubMed:
Citation:
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@article {pmid41800525,
year = {2026},
author = {Pai, YC and Yu, LC},
title = {Application of Artificial Intelligence-Powered Research in Gastrointestinal Pathophysiology: Unveiling Intestinal Pathobionts and Microbiota Dysbiosis.},
journal = {Journal of physiological investigation},
volume = {},
number = {},
pages = {},
pmid = {41800525},
issn = {2950-6344},
}
RevDate: 2026-03-09
Host-mediated Remodeling of the Gut Microbiota in Energy Homeostasis and Environmental Resilience.
Journal of physiological investigation pii:02275668-990000000-00060 [Epub ahead of print].
Additional Links: PMID-41800490
Publisher:
PubMed:
Citation:
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@article {pmid41800490,
year = {2026},
author = {Weng, YH and Chen, PC and Ruan, JW},
title = {Host-mediated Remodeling of the Gut Microbiota in Energy Homeostasis and Environmental Resilience.},
journal = {Journal of physiological investigation},
volume = {},
number = {},
pages = {},
doi = {10.4103/ejpi.EJPI-D-25-00028},
pmid = {41800490},
issn = {2950-6344},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Carrier-free supramolecular architectonics of quercetin-berberine for safety-redefined therapy of ulcerative colitis.
Materials today. Bio, 37:102970.
Ulcerative colitis (UC) poses significant clinical management challenges due to the limited efficacy and substantial safety burdens of existing treatments. This study develops a carrier-free supramolecular nanoassembly (QB) composed solely of quercetin (QU) and berberine (BBR), reshaping the safety-efficacy profile of these natural drugs at the nanoscale. Spectroscopic characterization and molecular dynamics simulations reveal that QU and BBR synergistically self-assemble into stable nanoparticles driven primarily by hydrogen bonding and π-π stacking, resulting in a highly negative surface charge and superior colloidal stability. In vitro and in vivo experiments demonstrate that QB markedly reduces BBR's cytotoxicity, expanding its therapeutic dose window by approximately 16-fold, while concurrently enhancing anti-inflammatory, antioxidant, and epithelial barrier repair effects in LPS-stimulated macrophages and DSS-induced UC mice. In vivo fluorescence imaging and tissue distribution indicate selective accumulation of orally administered QB in the inflamed colon and spleen, suggesting dual local intestinal and systemic immune modulatory capabilities. Transcriptomic and gut microbiome analyses further uncover QB's coordinated downregulation of inflammation-related signaling pathways, upregulation of metabolic and antioxidant modules, and restoration of microbial diversity and community homeostasis. Compared to QU or BBR monotherapy and 5-aminosalicylic acid, QB exhibits superior overall efficacy in alleviating colitis symptoms and tissue damage, with excellent biocompatibility, offering a scalable platform for safety-redefined, multidimensional precision interventions in UC based on natural small-molecule self-assembly.
Additional Links: PMID-41800457
PubMed:
Citation:
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@article {pmid41800457,
year = {2026},
author = {Zhang, X and Fu, Y and Liu, S and Zhang, J and Xu, F and Zhang, C and Wang, Y and Huo, C},
title = {Carrier-free supramolecular architectonics of quercetin-berberine for safety-redefined therapy of ulcerative colitis.},
journal = {Materials today. Bio},
volume = {37},
number = {},
pages = {102970},
pmid = {41800457},
issn = {2590-0064},
abstract = {Ulcerative colitis (UC) poses significant clinical management challenges due to the limited efficacy and substantial safety burdens of existing treatments. This study develops a carrier-free supramolecular nanoassembly (QB) composed solely of quercetin (QU) and berberine (BBR), reshaping the safety-efficacy profile of these natural drugs at the nanoscale. Spectroscopic characterization and molecular dynamics simulations reveal that QU and BBR synergistically self-assemble into stable nanoparticles driven primarily by hydrogen bonding and π-π stacking, resulting in a highly negative surface charge and superior colloidal stability. In vitro and in vivo experiments demonstrate that QB markedly reduces BBR's cytotoxicity, expanding its therapeutic dose window by approximately 16-fold, while concurrently enhancing anti-inflammatory, antioxidant, and epithelial barrier repair effects in LPS-stimulated macrophages and DSS-induced UC mice. In vivo fluorescence imaging and tissue distribution indicate selective accumulation of orally administered QB in the inflamed colon and spleen, suggesting dual local intestinal and systemic immune modulatory capabilities. Transcriptomic and gut microbiome analyses further uncover QB's coordinated downregulation of inflammation-related signaling pathways, upregulation of metabolic and antioxidant modules, and restoration of microbial diversity and community homeostasis. Compared to QU or BBR monotherapy and 5-aminosalicylic acid, QB exhibits superior overall efficacy in alleviating colitis symptoms and tissue damage, with excellent biocompatibility, offering a scalable platform for safety-redefined, multidimensional precision interventions in UC based on natural small-molecule self-assembly.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Health benefits of Bifidobacterium animalis subsp. lactis BB-12 in infants and children: a mini-review.
Frontiers in microbiology, 17:1773473.
The colonization of the infant gut microbiome during the critical window of 0-3 years is influenced by a multitude of prenatal, environmental and host factors, and may be crucial for life-long health. The infant gut microbiome is highly dynamic, with bifidobacteria-dominance generally established during birth and lactation, followed by transition to a more stable and adult-like composition reached around 3 years of age. Bifidobacteria-dominance in infancy is considered protective as they not only display both anti-inflammatory and immunomodulatory effects but also foster the establishment of other beneficial species via cross-feeding interactions. As predominance of bifidobacteria is considered the marker of a healthy breastfed infant, the use of bifidobacteria-based probiotics for the prevention of gut dysbiosis and related conditions has been investigated. This clinically oriented summary highlights the unmet research needs of Bifidobacterium animalis subsp. lactis, BB-12[®] (BB-12), a well-studied probiotic added to baby formulas, dietary supplements, and fermented milk products; several potentially beneficial attributes, including acid and bile tolerance, strong adherence properties, pathogen inhibition, and immune modulation are considered. Clinical studies have demonstrated the safety and beneficial effects of BB-12 in infants and children across multiple disorders and highlight the need for improved clinical and regulatory guidelines.
Additional Links: PMID-41800422
PubMed:
Citation:
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@article {pmid41800422,
year = {2026},
author = {Bueno, CPAR and Domínguez, AC and Guyonnet, D and Pouteau, E},
title = {Health benefits of Bifidobacterium animalis subsp. lactis BB-12 in infants and children: a mini-review.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1773473},
pmid = {41800422},
issn = {1664-302X},
abstract = {The colonization of the infant gut microbiome during the critical window of 0-3 years is influenced by a multitude of prenatal, environmental and host factors, and may be crucial for life-long health. The infant gut microbiome is highly dynamic, with bifidobacteria-dominance generally established during birth and lactation, followed by transition to a more stable and adult-like composition reached around 3 years of age. Bifidobacteria-dominance in infancy is considered protective as they not only display both anti-inflammatory and immunomodulatory effects but also foster the establishment of other beneficial species via cross-feeding interactions. As predominance of bifidobacteria is considered the marker of a healthy breastfed infant, the use of bifidobacteria-based probiotics for the prevention of gut dysbiosis and related conditions has been investigated. This clinically oriented summary highlights the unmet research needs of Bifidobacterium animalis subsp. lactis, BB-12[®] (BB-12), a well-studied probiotic added to baby formulas, dietary supplements, and fermented milk products; several potentially beneficial attributes, including acid and bile tolerance, strong adherence properties, pathogen inhibition, and immune modulation are considered. Clinical studies have demonstrated the safety and beneficial effects of BB-12 in infants and children across multiple disorders and highlight the need for improved clinical and regulatory guidelines.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Dynamic remodeling of skin microbiota during healthy homeostatic and wound repair conditions.
Frontiers in microbiology, 17:1781606.
The skin microbiota is a fundamental component of the cutaneous ecosystem and plays an important role in maintaining skin homeostasis through immune education, maintenance of the skin barrier, colonization resistance, and regulation of the physiological environment under healthy conditions. Skin injury disrupts this balanced microbial ecosystem, resulting in marked changes in the local microenvironment. However, the processes by which skin microbiota reorganise following injury and contribute to the restoration of a remodelled homeostatic ecosystem after wound repair are not fully understood. This review synthesizes current knowledge on host-microbiota interactions across the dynamic transition from healthy skin to wounded skin and to remodeled homeostatic skin. We highlight the functions of commensal microorganisms during the inflammatory, proliferative, and remodeling phases of wound healing, with a particular focus on their roles in the resolution of inflammation, tissue regeneration and barrier restoration. Finally, we discuss emerging microbiota-based therapeutic opportunities for wound management and outline key challenges and future research directions aimed at promoting long-term restoration of skin microbial homeostasis.
Additional Links: PMID-41800418
PubMed:
Citation:
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@article {pmid41800418,
year = {2026},
author = {Ye, H and Wong, A and Chen, X and Sun, W and He, H and Li, X and Wu, J},
title = {Dynamic remodeling of skin microbiota during healthy homeostatic and wound repair conditions.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1781606},
pmid = {41800418},
issn = {1664-302X},
abstract = {The skin microbiota is a fundamental component of the cutaneous ecosystem and plays an important role in maintaining skin homeostasis through immune education, maintenance of the skin barrier, colonization resistance, and regulation of the physiological environment under healthy conditions. Skin injury disrupts this balanced microbial ecosystem, resulting in marked changes in the local microenvironment. However, the processes by which skin microbiota reorganise following injury and contribute to the restoration of a remodelled homeostatic ecosystem after wound repair are not fully understood. This review synthesizes current knowledge on host-microbiota interactions across the dynamic transition from healthy skin to wounded skin and to remodeled homeostatic skin. We highlight the functions of commensal microorganisms during the inflammatory, proliferative, and remodeling phases of wound healing, with a particular focus on their roles in the resolution of inflammation, tissue regeneration and barrier restoration. Finally, we discuss emerging microbiota-based therapeutic opportunities for wound management and outline key challenges and future research directions aimed at promoting long-term restoration of skin microbial homeostasis.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Impact of non-standardized reporting on reproducibility, usability, and integration in nasopharyngeal metagenomic research: a systematic review.
Frontiers in microbiology, 17:1707004.
INTRODUCTION: The nasopharyngeal microbiome plays a critical role in respiratory health and disease and is a major focus of metagenomic research. However, inconsistent reporting practices across studies limit reproducibility, dataset usability, and cross-study integration, thereby reducing the overall scientific value of publicly available nasopharyn.
METHODS: A systematic review was conducted to evaluate the impact of non-standardized reporting on reproducibility, usability, and integration of nasopharyngeal metagenomic datasets. A total of 988 studies were screened, and 227 manuscripts met predefined inclusion and exclusion criteria for full-text review. Methodological reproducibility, metadata completeness, and compatibility between reported laboratory methods and deposited datasets were assessed. Reproducible datasets were further analyzed to evaluate the interchangeability of nasopharyngeal aspirates and nasopharyngeal swabs.
RESULTS: Only 78 studies (34%) contained methods sections sufficient for reproducibility, and of these, 33 studies (15%) provided analytically sufficient metadata to support secondary analysis. Mismatches between reported laboratory methods and deposited datasets were identified in 4% of studies. These deficiencies were primarily attributed to incomplete methodological reporting, inaccessible or insufficient metadata, and incompatible file formats. Comparative analysis of reproducible datasets demonstrated significant differences in microbial profiles between nasopharyngeal aspirates and nasopharyngeal swabs, confirming that these specimen types are not interchangeable within a study.
DISCUSSION: The findings demonstrate that inadequate reporting standards substantially impair the reproducibility, reuse, and integration of nasopharyngeal metagenomic data. The observed methodological and metadata inconsistencies limit the reliability of downstream analyses and cross-study comparisons. Standardized reporting guidelines are urgently needed to improve transparency, ensure reproducibility, and enhance the integrative potential of nasopharyngeal microbiome research. Adoption of comprehensive and consistent reporting practices would significantly strengthen the scientific rigor and utility of metagenomic studies in this field.
Additional Links: PMID-41800416
PubMed:
Citation:
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@article {pmid41800416,
year = {2026},
author = {Bustos, ML and Song, K and Brochu, HN and Zhang, Q and Iyer, LK and Icenhour, CR},
title = {Impact of non-standardized reporting on reproducibility, usability, and integration in nasopharyngeal metagenomic research: a systematic review.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1707004},
pmid = {41800416},
issn = {1664-302X},
abstract = {INTRODUCTION: The nasopharyngeal microbiome plays a critical role in respiratory health and disease and is a major focus of metagenomic research. However, inconsistent reporting practices across studies limit reproducibility, dataset usability, and cross-study integration, thereby reducing the overall scientific value of publicly available nasopharyn.
METHODS: A systematic review was conducted to evaluate the impact of non-standardized reporting on reproducibility, usability, and integration of nasopharyngeal metagenomic datasets. A total of 988 studies were screened, and 227 manuscripts met predefined inclusion and exclusion criteria for full-text review. Methodological reproducibility, metadata completeness, and compatibility between reported laboratory methods and deposited datasets were assessed. Reproducible datasets were further analyzed to evaluate the interchangeability of nasopharyngeal aspirates and nasopharyngeal swabs.
RESULTS: Only 78 studies (34%) contained methods sections sufficient for reproducibility, and of these, 33 studies (15%) provided analytically sufficient metadata to support secondary analysis. Mismatches between reported laboratory methods and deposited datasets were identified in 4% of studies. These deficiencies were primarily attributed to incomplete methodological reporting, inaccessible or insufficient metadata, and incompatible file formats. Comparative analysis of reproducible datasets demonstrated significant differences in microbial profiles between nasopharyngeal aspirates and nasopharyngeal swabs, confirming that these specimen types are not interchangeable within a study.
DISCUSSION: The findings demonstrate that inadequate reporting standards substantially impair the reproducibility, reuse, and integration of nasopharyngeal metagenomic data. The observed methodological and metadata inconsistencies limit the reliability of downstream analyses and cross-study comparisons. Standardized reporting guidelines are urgently needed to improve transparency, ensure reproducibility, and enhance the integrative potential of nasopharyngeal microbiome research. Adoption of comprehensive and consistent reporting practices would significantly strengthen the scientific rigor and utility of metagenomic studies in this field.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Plant-soil-microbiome interactions: mechanisms, advances, and challenges in sustainable agriculture and healthy agroecosystems.
Frontiers in microbiology, 17:1762743.
The focus of this article is to summarize current knowledge of plant-associated microbiomes, which play a key role in plant health and in maintaining soil quality. Such microbiomes, comprising bacteria, fungi, archaea, algae, nematodes, and protists, perform various functions, including nutrient transformation, pathogen protection, and stress mitigation. Microbial communities are commonly used as an indicator of ecosystem health. Soil microbiome diversity depends on environmental factors (including biotic and abiotic stresses), which can alter microbial composition, thereby modifying microbial interactions and plant resilience. Biofertilizers, biopreparations, and microbial inoculants or consortia have been utilized in agriculture to enhance soil properties, such as microbial diversity and enzymatic activity, and to prime plant immune responses, thereby promoting plant growth and health. Biofertilizers can significantly help plants adapt to environmental stresses and climate change, mitigating drought stress and reducing greenhouse gas emissions. Recent advances in DNA sequencing technologies, the computing power available to scientists, and the development of bioinformatics tools have made microbial community studies widely accessible. These tools enable the research and modeling of changes in the soil microbiome, plant disease susceptibility, and soil health. Multi-omics approaches to microbiomes are key to characterizing the microbiome and predicting plant diseases. Future research should focus primarily on understanding the interactions among soil, plants, and microbiomes. This approach will help develop climate-resilient plants and improve the health and functionality of agroecosystems. Key efforts closely aligned with the European Union's goals and biodiversity strategies for sustainable agriculture and soil health restoration, as presented in this review, include studying the structures and functions of soil microbiomes, developing new assays, and designing and investigating microbial consortia to restore healthy communities. These strategies address contemporary challenges in agriculture, including vertical and urban farming and superfood production.
Additional Links: PMID-41800415
PubMed:
Citation:
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@article {pmid41800415,
year = {2026},
author = {Panek, J and Gryta, A and Maj, W and Mącik, M and Oszust, K and Pertile, G and Pylak, M and Siegieda, D and Hallama, M and Hatano, R and Kandeler, E and Pathan, SI and Pietramellara, G and Malusa, E and Weber, J and Turnau, K and Różalska, S and Frąc, M},
title = {Plant-soil-microbiome interactions: mechanisms, advances, and challenges in sustainable agriculture and healthy agroecosystems.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1762743},
pmid = {41800415},
issn = {1664-302X},
abstract = {The focus of this article is to summarize current knowledge of plant-associated microbiomes, which play a key role in plant health and in maintaining soil quality. Such microbiomes, comprising bacteria, fungi, archaea, algae, nematodes, and protists, perform various functions, including nutrient transformation, pathogen protection, and stress mitigation. Microbial communities are commonly used as an indicator of ecosystem health. Soil microbiome diversity depends on environmental factors (including biotic and abiotic stresses), which can alter microbial composition, thereby modifying microbial interactions and plant resilience. Biofertilizers, biopreparations, and microbial inoculants or consortia have been utilized in agriculture to enhance soil properties, such as microbial diversity and enzymatic activity, and to prime plant immune responses, thereby promoting plant growth and health. Biofertilizers can significantly help plants adapt to environmental stresses and climate change, mitigating drought stress and reducing greenhouse gas emissions. Recent advances in DNA sequencing technologies, the computing power available to scientists, and the development of bioinformatics tools have made microbial community studies widely accessible. These tools enable the research and modeling of changes in the soil microbiome, plant disease susceptibility, and soil health. Multi-omics approaches to microbiomes are key to characterizing the microbiome and predicting plant diseases. Future research should focus primarily on understanding the interactions among soil, plants, and microbiomes. This approach will help develop climate-resilient plants and improve the health and functionality of agroecosystems. Key efforts closely aligned with the European Union's goals and biodiversity strategies for sustainable agriculture and soil health restoration, as presented in this review, include studying the structures and functions of soil microbiomes, developing new assays, and designing and investigating microbial consortia to restore healthy communities. These strategies address contemporary challenges in agriculture, including vertical and urban farming and superfood production.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Multi-site microbiota crosstalk in the postmenopausal: from dysbiosis mechanisms to precision interventions.
Frontiers in microbiology, 17:1702700.
Persistent estrogen deficiency in postmenopause reshapes the gut-vaginal-urinary ecosystems, contributing to multisystem dysfunction through interconnected dysbiosis. Cross-niche microbial interactions amplify systemic risks: gut-derived toxins are linked to vascular inflammation, vaginal dysbiosis facilitates urinary pathogen colonization, and bile acid disruption impairs bone-immune homeostasis. This review synthesizes current mechanistic evidence illustrating how microbial networks propagate postmenopausal comorbidities. We propose the framework of "Postmenopausal Microbiota Network Medicine" which integrates microbial dynamics with host omics to transition from symptomatic management toward root-cause interception by strengthening microbial network resilience.
Additional Links: PMID-41800413
PubMed:
Citation:
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@article {pmid41800413,
year = {2026},
author = {Fang, J and He, X and Zhou, J},
title = {Multi-site microbiota crosstalk in the postmenopausal: from dysbiosis mechanisms to precision interventions.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1702700},
pmid = {41800413},
issn = {1664-302X},
abstract = {Persistent estrogen deficiency in postmenopause reshapes the gut-vaginal-urinary ecosystems, contributing to multisystem dysfunction through interconnected dysbiosis. Cross-niche microbial interactions amplify systemic risks: gut-derived toxins are linked to vascular inflammation, vaginal dysbiosis facilitates urinary pathogen colonization, and bile acid disruption impairs bone-immune homeostasis. This review synthesizes current mechanistic evidence illustrating how microbial networks propagate postmenopausal comorbidities. We propose the framework of "Postmenopausal Microbiota Network Medicine" which integrates microbial dynamics with host omics to transition from symptomatic management toward root-cause interception by strengthening microbial network resilience.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Microbial succession and tissue-specific restructuring of bacterial and fungal communities during post-harvest onion bulb rotting.
Frontiers in microbiology, 17:1776996.
Despite being a relatively hardy bulb crop with a longer shelf life than many fresh vegetables, onions are susceptible to substantial postharvest losses due to microbial spoilage. This study used high-throughput amplicon sequencing to characterize the bacterial and fungal microbiomes associated with healthy (HB), mildly rotten (MRB), and severely rotten (SRB) onion bulbs. Microbial communities were analysed across three distinct bulb tissues comprising neck tissue (NT), outer scale (OS), and central tissue (CT), to generate stage-specific and tissue-specific microbiome profiles. The microbial community analysis based on over 2 million Illumina NGS reads revealed the presence of 85 bacterial OTUs and 53 fungal OTUs across nine bulb samples. Bulb deterioration was marked by pronounced microbial succession, with bacterial diversity increasing from healthy bulbs (8 genera) to mildly rotten bulbs (36 genera), followed by a sharp decline in severely rotten bulbs (11 genera). Several bacterial genera, including Lactobacillus, Novosphingobium, Sphingobium, Pluralibacter, Acetobacter, Gluconobacter and Pantoea, emerged exclusively in rotten bulbs and were absent in healthy tissues, indicating their association with the onion bulb rot. The microbiome of SRB was marked by an overwhelming dominance of Lactobacillus (33.2% in SRB-CT, 16.9% in SRB-NT, 10.8% in SRB-OS), Acetobacter (16.1% in SRB-CT, 15.6% in SRB-NT, 7.0% in SRB-OS), Carnimonas (57.0% in SRB-NT), and Gluconobacter (14.5% in SRB-OS). Fungal communities exhibited a similar successional pattern: healthy bulbs showed negligible fungal presence except in the neck tissue (HB-NT), whereas mildly rotten bulbs showed a sharp increase in fungal diversity dominated by Meyerozyma (21.7%), Blastobotrys (13.3%), and Penicillium (7.0%). In severely rotten bulbs, fungal diversity declined, with Pichia (48.3%) and Kazachstania (8.6%) becoming dominant. Differential abundance analysis using edgeR identified six bacterial genera (Lactobacillus, Novosphingobium, Acetobacter, Pluralibacter, Carnimonas, and Dysgonomonas) and two fungal genera (Pichia and Kazachstania) that exhibited significant stage-dependent shifts during bulb rot progression. Alpha- and beta-diversity analyses revealed strong tissue-specific structuring of fungal communities, identifying the neck region as the primary fungal succession zone. Overall, this study elucidates the ecological restructuring of bacterial and fungal communities during onion bulb deterioration, and would pave the way for devising microbiome-informed interventions to reduce postharvest losses in onions.
Additional Links: PMID-41800410
PubMed:
Citation:
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@article {pmid41800410,
year = {2026},
author = {Kumar, S and Dutta, R and Auji, R and Wackchaure, GC and Jayalakshmi, K and Karuppaiah, V and Mahajan, V},
title = {Microbial succession and tissue-specific restructuring of bacterial and fungal communities during post-harvest onion bulb rotting.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1776996},
pmid = {41800410},
issn = {1664-302X},
abstract = {Despite being a relatively hardy bulb crop with a longer shelf life than many fresh vegetables, onions are susceptible to substantial postharvest losses due to microbial spoilage. This study used high-throughput amplicon sequencing to characterize the bacterial and fungal microbiomes associated with healthy (HB), mildly rotten (MRB), and severely rotten (SRB) onion bulbs. Microbial communities were analysed across three distinct bulb tissues comprising neck tissue (NT), outer scale (OS), and central tissue (CT), to generate stage-specific and tissue-specific microbiome profiles. The microbial community analysis based on over 2 million Illumina NGS reads revealed the presence of 85 bacterial OTUs and 53 fungal OTUs across nine bulb samples. Bulb deterioration was marked by pronounced microbial succession, with bacterial diversity increasing from healthy bulbs (8 genera) to mildly rotten bulbs (36 genera), followed by a sharp decline in severely rotten bulbs (11 genera). Several bacterial genera, including Lactobacillus, Novosphingobium, Sphingobium, Pluralibacter, Acetobacter, Gluconobacter and Pantoea, emerged exclusively in rotten bulbs and were absent in healthy tissues, indicating their association with the onion bulb rot. The microbiome of SRB was marked by an overwhelming dominance of Lactobacillus (33.2% in SRB-CT, 16.9% in SRB-NT, 10.8% in SRB-OS), Acetobacter (16.1% in SRB-CT, 15.6% in SRB-NT, 7.0% in SRB-OS), Carnimonas (57.0% in SRB-NT), and Gluconobacter (14.5% in SRB-OS). Fungal communities exhibited a similar successional pattern: healthy bulbs showed negligible fungal presence except in the neck tissue (HB-NT), whereas mildly rotten bulbs showed a sharp increase in fungal diversity dominated by Meyerozyma (21.7%), Blastobotrys (13.3%), and Penicillium (7.0%). In severely rotten bulbs, fungal diversity declined, with Pichia (48.3%) and Kazachstania (8.6%) becoming dominant. Differential abundance analysis using edgeR identified six bacterial genera (Lactobacillus, Novosphingobium, Acetobacter, Pluralibacter, Carnimonas, and Dysgonomonas) and two fungal genera (Pichia and Kazachstania) that exhibited significant stage-dependent shifts during bulb rot progression. Alpha- and beta-diversity analyses revealed strong tissue-specific structuring of fungal communities, identifying the neck region as the primary fungal succession zone. Overall, this study elucidates the ecological restructuring of bacterial and fungal communities during onion bulb deterioration, and would pave the way for devising microbiome-informed interventions to reduce postharvest losses in onions.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Divergent sucker-corm endophytic microbiota underpins the progressive decline of Fusarium-wilt incidence in resistant bananas across ratoon cycles.
Frontiers in microbiology, 17:1676292.
Fusarium wilt of banana, caused by Fusarium oxysporum f. sp. cubense (Foc), threatens global banana production. Resistant cultivars exhibit reduced disease incidence after successive ratoon cycles, but the underlying micro-ecological mechanisms remain unclear. This study represents the first longitudinal analysis of corm endophytic microbiota across ratoon cycles in banana, revealing temporal dynamics that underpin progressive disease resistance. A three-cycle field trial with three biological replicates per cultivar per cycle was conducted in a Foc-infested orchard in Guangxi, China. Corm tissues were sampled from resistant ('Bao Dao Jiao' and 'Gui Jiao 9') and susceptible 'Williams B6' bananas (n = 3 biological replicates per group) at plant crop (cycle 1) and third ratoon (cycle 3). 16S rRNA amplicons were sequenced via Illumina NovaSeq. Alpha- and beta-diversity, taxonomic composition, and predicted functions (PICRUSt2) were analyzed. Resistant cultivars maintained significantly higher Chao1 and Shannon indices than the susceptible cultivar, with divergence intensified across ratoon cycles (p < 0.05). Community structure was shaped primarily by cultivar rather than maternal health status. Resistant genotypes enriched Proteobacteria and Actinobacteria, alongside beneficial genera (Halomonas, Nesterenkonia, Aliihoeflea). Functional predictions revealed enrichment in carbohydrate metabolism, membrane transport, and xenobiotic degradation pathways in resistant cultivars. Disease incidence declined significantly from 34-39% (cycle 1) to 4-8% (cycle 3) in resistant cultivars, whereas susceptible cultivars remained at 44-59%. Resistant bananas continuously recruit beneficial endophytes during ratooning, assembling a stable microbiome that reinforces Fusarium wilt resistance. These findings provide microbial targets for breeding and biocontrol strategies.
Additional Links: PMID-41800399
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Citation:
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@article {pmid41800399,
year = {2026},
author = {Xiang, S and Tian, D and Chen, J and He, Z and Wei, L and Qin, L and Li, C and Li, B},
title = {Divergent sucker-corm endophytic microbiota underpins the progressive decline of Fusarium-wilt incidence in resistant bananas across ratoon cycles.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1676292},
pmid = {41800399},
issn = {1664-302X},
abstract = {Fusarium wilt of banana, caused by Fusarium oxysporum f. sp. cubense (Foc), threatens global banana production. Resistant cultivars exhibit reduced disease incidence after successive ratoon cycles, but the underlying micro-ecological mechanisms remain unclear. This study represents the first longitudinal analysis of corm endophytic microbiota across ratoon cycles in banana, revealing temporal dynamics that underpin progressive disease resistance. A three-cycle field trial with three biological replicates per cultivar per cycle was conducted in a Foc-infested orchard in Guangxi, China. Corm tissues were sampled from resistant ('Bao Dao Jiao' and 'Gui Jiao 9') and susceptible 'Williams B6' bananas (n = 3 biological replicates per group) at plant crop (cycle 1) and third ratoon (cycle 3). 16S rRNA amplicons were sequenced via Illumina NovaSeq. Alpha- and beta-diversity, taxonomic composition, and predicted functions (PICRUSt2) were analyzed. Resistant cultivars maintained significantly higher Chao1 and Shannon indices than the susceptible cultivar, with divergence intensified across ratoon cycles (p < 0.05). Community structure was shaped primarily by cultivar rather than maternal health status. Resistant genotypes enriched Proteobacteria and Actinobacteria, alongside beneficial genera (Halomonas, Nesterenkonia, Aliihoeflea). Functional predictions revealed enrichment in carbohydrate metabolism, membrane transport, and xenobiotic degradation pathways in resistant cultivars. Disease incidence declined significantly from 34-39% (cycle 1) to 4-8% (cycle 3) in resistant cultivars, whereas susceptible cultivars remained at 44-59%. Resistant bananas continuously recruit beneficial endophytes during ratooning, assembling a stable microbiome that reinforces Fusarium wilt resistance. These findings provide microbial targets for breeding and biocontrol strategies.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Trehalose-mediated reshaping of the rhizosphere microbiome drives tea root rot progression.
Frontiers in microbiology, 17:1787317.
Tea (Camellia sinensis [L.] Kuntze) is one of the most economically important crops and as a traditional medicinal plant in the world. The long-term continuous cropping and inappropriate management have led to frequent outbreaks of soil-borne diseases such as root rot, which pose a serious threat to the sustainable development of the tea industry. However, the pathogenesis of tea root rot remains poorly understood. In this study, two novel pathogen fungi, Paraconiothyrium cyclothyrioides F8 and Apiotrichum sporotrichoides F17, were isolated and identified from diseased tea roots. Microbiome analysis revealed significant restructuring of the rhizosphere microbial community in diseased tea plants, with a significant reduction in the abundance of Basidiomycota and marked enrichment of pathogen such as Fusarium and Apiotrichum. Meanwhile, the abundances of beneficial fungi (e.g., Saitozyma and Trichoderma) and bacteria (e.g., Bacillus and Sporosarcina) were significantly decreased. Further investigation demonstrated that root exudate trehalose exhibited prominent bidirectional regulatory effect through promoted the growth of pathogen, while simultaneously inhibiting biofilm formation, rhizosphere colonization at specific concentrations and weakened the biocontrol functions of the beneficial antagonistic bacteria Sporosarcina pasteurii T21 and Lysinibacillus sp. T23, facilitating the formation of a rhizosphere chemical environment that "aids enemies and harms allies" and thereby exacerbating disease occurrence. This study emphasized the dominant role of plant metabolites such as trehalose in driving the assembly of rhizosphere microbial communities from a disease-suppressive to a disease-conducive state, as well as in disease development. The findings provide a novel theoretical perspective for the microbiological regulation of tea root rot and offer theoretical and practical bases for tea root rot disease green prevention and control.
Additional Links: PMID-41800398
PubMed:
Citation:
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@article {pmid41800398,
year = {2026},
author = {Zhu, Q and Chen, B and Hu, W and Huang, Y and Wang, S and Feng, M and Zhao, J and Yu, M and Li, M and Gong, X},
title = {Trehalose-mediated reshaping of the rhizosphere microbiome drives tea root rot progression.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1787317},
pmid = {41800398},
issn = {1664-302X},
abstract = {Tea (Camellia sinensis [L.] Kuntze) is one of the most economically important crops and as a traditional medicinal plant in the world. The long-term continuous cropping and inappropriate management have led to frequent outbreaks of soil-borne diseases such as root rot, which pose a serious threat to the sustainable development of the tea industry. However, the pathogenesis of tea root rot remains poorly understood. In this study, two novel pathogen fungi, Paraconiothyrium cyclothyrioides F8 and Apiotrichum sporotrichoides F17, were isolated and identified from diseased tea roots. Microbiome analysis revealed significant restructuring of the rhizosphere microbial community in diseased tea plants, with a significant reduction in the abundance of Basidiomycota and marked enrichment of pathogen such as Fusarium and Apiotrichum. Meanwhile, the abundances of beneficial fungi (e.g., Saitozyma and Trichoderma) and bacteria (e.g., Bacillus and Sporosarcina) were significantly decreased. Further investigation demonstrated that root exudate trehalose exhibited prominent bidirectional regulatory effect through promoted the growth of pathogen, while simultaneously inhibiting biofilm formation, rhizosphere colonization at specific concentrations and weakened the biocontrol functions of the beneficial antagonistic bacteria Sporosarcina pasteurii T21 and Lysinibacillus sp. T23, facilitating the formation of a rhizosphere chemical environment that "aids enemies and harms allies" and thereby exacerbating disease occurrence. This study emphasized the dominant role of plant metabolites such as trehalose in driving the assembly of rhizosphere microbial communities from a disease-suppressive to a disease-conducive state, as well as in disease development. The findings provide a novel theoretical perspective for the microbiological regulation of tea root rot and offer theoretical and practical bases for tea root rot disease green prevention and control.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
OmniCorr: an R-package for visualizing putative host-microbiome interactions using multi-omics data.
Bioinformatics advances, 6(1):vbag057.
Holo-omics leverages omics datasets to explore the interactions between hosts and their associated microbiomes. Although the generation of omics data from matching host and microbiome samples is steadily increasing, there remains a scarcity of computational tools capable of integrating and visualizing this data to facilitate the prediction and interpretation of host-microbiome interactions. We present OmniCorr, an R package designed to: (i) manage the complexity of omics data by clustering co-varying features (e.g. genes, proteins, and metabolites) into modules, (ii) visualize correlations of these modules across different omics layers, host-microbiome interfaces, and metadata, and (iii) identify statistically significant associations indicative of putative host-microbiome interactions. OmniCorr's utility is demonstrated using datasets from two systems: (i) Atlantic salmon, integrating host transcriptomics with metagenomics and metatranscriptomics to explore dietary impacts, and (ii) cattle, combining host proteomics with metaproteomics to investigate methane emission variability. Availability and implementation: OmniCorr is freely available at https://github.com/shashank-KU/OmniCorr.
Additional Links: PMID-41800387
PubMed:
Citation:
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@article {pmid41800387,
year = {2026},
author = {Gupta, S and Quarato, V and Lai, W and Kobel, CM and Aho, VTE and Vera-Ponce de León, A and La Rosa, SL and Sandve, SR and Pope, PB and Hvidsten, TR},
title = {OmniCorr: an R-package for visualizing putative host-microbiome interactions using multi-omics data.},
journal = {Bioinformatics advances},
volume = {6},
number = {1},
pages = {vbag057},
pmid = {41800387},
issn = {2635-0041},
abstract = {Holo-omics leverages omics datasets to explore the interactions between hosts and their associated microbiomes. Although the generation of omics data from matching host and microbiome samples is steadily increasing, there remains a scarcity of computational tools capable of integrating and visualizing this data to facilitate the prediction and interpretation of host-microbiome interactions. We present OmniCorr, an R package designed to: (i) manage the complexity of omics data by clustering co-varying features (e.g. genes, proteins, and metabolites) into modules, (ii) visualize correlations of these modules across different omics layers, host-microbiome interfaces, and metadata, and (iii) identify statistically significant associations indicative of putative host-microbiome interactions. OmniCorr's utility is demonstrated using datasets from two systems: (i) Atlantic salmon, integrating host transcriptomics with metagenomics and metatranscriptomics to explore dietary impacts, and (ii) cattle, combining host proteomics with metaproteomics to investigate methane emission variability. Availability and implementation: OmniCorr is freely available at https://github.com/shashank-KU/OmniCorr.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
TAGINE: fast taxonomy-based feature engineering for microbiome analysis.
Bioinformatics advances, 6(1):vbag056.
SUMMARY: TAGINE is a feature engineering algorithm that leverages the microbial taxonomic tree to optimize feature sets in microbiome data for predictive modeling. The algorithm starts with features at high taxonomic levels and iteratively splits them into lower-level clades in cases where it improves predictive accuracy, ultimately producing a feature set spanning multiple taxonomic levels. This approach aims to markedly reduce the number of features while preserving biological relevance and interpretability. We compare TAGINE's performance to other standard and taxonomy-based feature engineering methods on several different datasets, and show that TAGINE yields more compact feature sets and is orders of magnitude faster than other methods, while maintaining predictive accuracy.
TAGINE is freely available under the MIT license with source code available at https://github.com/borenstein-lab/tagine_fe.
Additional Links: PMID-41800386
PubMed:
Citation:
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@article {pmid41800386,
year = {2026},
author = {Baum, S and Meshulam, I and Algavi, YM and Peleg, O and Borenstein, E},
title = {TAGINE: fast taxonomy-based feature engineering for microbiome analysis.},
journal = {Bioinformatics advances},
volume = {6},
number = {1},
pages = {vbag056},
pmid = {41800386},
issn = {2635-0041},
abstract = {SUMMARY: TAGINE is a feature engineering algorithm that leverages the microbial taxonomic tree to optimize feature sets in microbiome data for predictive modeling. The algorithm starts with features at high taxonomic levels and iteratively splits them into lower-level clades in cases where it improves predictive accuracy, ultimately producing a feature set spanning multiple taxonomic levels. This approach aims to markedly reduce the number of features while preserving biological relevance and interpretability. We compare TAGINE's performance to other standard and taxonomy-based feature engineering methods on several different datasets, and show that TAGINE yields more compact feature sets and is orders of magnitude faster than other methods, while maintaining predictive accuracy.
TAGINE is freely available under the MIT license with source code available at https://github.com/borenstein-lab/tagine_fe.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Gut-Lung Microbiota Axis Shapes the Immune Microenvironment and Immunotherapeutic Response in Lung Cancer.
International journal of biological sciences, 22(5):2265-2284.
The gut-lung axis microbiota plays a pivotal role in shaping the tumor immune microenvironment (TIME) and regulating immunotherapeutic responses in lung cancer. This review highlights that pulmonary and gut microbial dysbiosis drives lung cancer development through inducing chronic inflammation, remodeling the immune microenvironment, and reprogramming metabolism. Lung cancer patients exhibit distinct microbial signatures characterized by altered microbiotal diversity and enrichment of specific taxa like Streptococcus, Veillonella, and Bacteroidetes in the airways, along with gut microbial shifts involving decreased Firmicutes/Bacteroidetes ratio. These microbial alterations promote tumor progression via activation of pro-inflammatory pathways (e.g., interleukin-17 (IL-17)/interleukin-23 (IL-23) axis) and suppression of antitumor immunity.Notably, the gut-lung microbiome exerts a profound impact on immunotherapeutic efficacy: responders are enriched with beneficial microbes like Akkermansia muciniphila and Bifidobacterium that enhance CD8[+] T cell responses, while non-responders show elevated levels of Gammaproteobacteria and Fusobacterium associated with immunosuppression. Regulatory mechanisms include systemic immune modulation by microbial metabolites such as short-chain fatty acids, as well as activation of key signaling pathways including cGAS-STING and CD40L-CD40/NF-κB. Emerging translational applications encompass lung cancer diagnosis and immunotherapeutic response prediction via microbial biomarkers, as well as therapeutic interventions including fecal microbiota transplantation (FMT) and probiotic supplementation. Future studies should clarify microbe-host interaction mechanisms and develop personalized microbiota-based strategies to overcome immunotherapy resistance, offering the potential to revolutionize precision oncology through integrating microbiota modulation with conventional therapies.
Additional Links: PMID-41800246
PubMed:
Citation:
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@article {pmid41800246,
year = {2026},
author = {Liu, Y and Wang, S and Xiang, X and Du, Y and Xue, Q and Niu, Y and Peng, W and Ye, L and Zhou, Q},
title = {Gut-Lung Microbiota Axis Shapes the Immune Microenvironment and Immunotherapeutic Response in Lung Cancer.},
journal = {International journal of biological sciences},
volume = {22},
number = {5},
pages = {2265-2284},
pmid = {41800246},
issn = {1449-2288},
mesh = {Humans ; *Lung Neoplasms/immunology/therapy/microbiology ; *Gastrointestinal Microbiome/physiology/immunology ; *Tumor Microenvironment/immunology ; *Immunotherapy/methods ; *Lung/microbiology/immunology ; Dysbiosis ; Animals ; },
abstract = {The gut-lung axis microbiota plays a pivotal role in shaping the tumor immune microenvironment (TIME) and regulating immunotherapeutic responses in lung cancer. This review highlights that pulmonary and gut microbial dysbiosis drives lung cancer development through inducing chronic inflammation, remodeling the immune microenvironment, and reprogramming metabolism. Lung cancer patients exhibit distinct microbial signatures characterized by altered microbiotal diversity and enrichment of specific taxa like Streptococcus, Veillonella, and Bacteroidetes in the airways, along with gut microbial shifts involving decreased Firmicutes/Bacteroidetes ratio. These microbial alterations promote tumor progression via activation of pro-inflammatory pathways (e.g., interleukin-17 (IL-17)/interleukin-23 (IL-23) axis) and suppression of antitumor immunity.Notably, the gut-lung microbiome exerts a profound impact on immunotherapeutic efficacy: responders are enriched with beneficial microbes like Akkermansia muciniphila and Bifidobacterium that enhance CD8[+] T cell responses, while non-responders show elevated levels of Gammaproteobacteria and Fusobacterium associated with immunosuppression. Regulatory mechanisms include systemic immune modulation by microbial metabolites such as short-chain fatty acids, as well as activation of key signaling pathways including cGAS-STING and CD40L-CD40/NF-κB. Emerging translational applications encompass lung cancer diagnosis and immunotherapeutic response prediction via microbial biomarkers, as well as therapeutic interventions including fecal microbiota transplantation (FMT) and probiotic supplementation. Future studies should clarify microbe-host interaction mechanisms and develop personalized microbiota-based strategies to overcome immunotherapy resistance, offering the potential to revolutionize precision oncology through integrating microbiota modulation with conventional therapies.},
}
MeSH Terms:
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Humans
*Lung Neoplasms/immunology/therapy/microbiology
*Gastrointestinal Microbiome/physiology/immunology
*Tumor Microenvironment/immunology
*Immunotherapy/methods
*Lung/microbiology/immunology
Dysbiosis
Animals
RevDate: 2026-03-09
CmpDate: 2026-03-09
Harnessing the Gut Microbiota to Improve Cancer Immunotherapy: Focus on Lung Cancer.
Immune network, 26(1):e7.
The gut microbiota has emerged as a key orchestrator of systemic immunity, capable of reshaping the tumor microenvironment and modulating responses to cancer immunotherapy via the gut-lung axis. While immune checkpoint blockade (ICB) has revolutionized lung cancer treatment, a significant proportion of patients fail to respond. Accumulating evidence suggests that intestinal microbial composition modulates antitumor immunity, yet clinical associations between specific microbial taxa and ICB outcomes often show inconsistencies across cohorts. In this review, we synthesize current mechanistic insights into how gut microbial metabolites and structural components modulate pulmonary immune surveillance. We critically examine the clinical landscape of microbiome signatures in non-small cell lung cancer (NSCLC), highlighting how species- and strain-level heterogeneity contributes to divergent findings. Finally, we discuss translational strategies-ranging from fecal microbiota transplantation to rationally designed bacterial consortia and engineered probiotics-and propose a roadmap for integrating multi-omics with microbiome engineering to overcome current limitations and optimize precision immunotherapy.
Additional Links: PMID-41800020
PubMed:
Citation:
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@article {pmid41800020,
year = {2026},
author = {Park, U and Heo, JY and Chun, SM and Lee, JC and Lee, SH and Lee, SW},
title = {Harnessing the Gut Microbiota to Improve Cancer Immunotherapy: Focus on Lung Cancer.},
journal = {Immune network},
volume = {26},
number = {1},
pages = {e7},
pmid = {41800020},
issn = {1598-2629},
abstract = {The gut microbiota has emerged as a key orchestrator of systemic immunity, capable of reshaping the tumor microenvironment and modulating responses to cancer immunotherapy via the gut-lung axis. While immune checkpoint blockade (ICB) has revolutionized lung cancer treatment, a significant proportion of patients fail to respond. Accumulating evidence suggests that intestinal microbial composition modulates antitumor immunity, yet clinical associations between specific microbial taxa and ICB outcomes often show inconsistencies across cohorts. In this review, we synthesize current mechanistic insights into how gut microbial metabolites and structural components modulate pulmonary immune surveillance. We critically examine the clinical landscape of microbiome signatures in non-small cell lung cancer (NSCLC), highlighting how species- and strain-level heterogeneity contributes to divergent findings. Finally, we discuss translational strategies-ranging from fecal microbiota transplantation to rationally designed bacterial consortia and engineered probiotics-and propose a roadmap for integrating multi-omics with microbiome engineering to overcome current limitations and optimize precision immunotherapy.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Metagenomics as an Effective Diagnostic Approach for Exploring Oral Microbial Diversity and Dental Diseases: A Narrative Review.
International journal of clinical pediatric dentistry, 19(2):278-284.
AIM AND BACKGROUND: The oral cavity harbors a diverse microbiota that significantly influences oral health and disease. Conventional microbiological techniques have limitations in detecting the full range of microbial species, particularly those that are uncultivable. Metagenomics, through culture-independent, high-throughput sequencing methods, offers a comprehensive approach to studying oral microbial diversity. This narrative review aims to evaluate the role of metagenomics in exploring the oral microbiome and its association with dental diseases.
METHODS: This review systematically synthesized current literature and research on metagenomic technologies, including 16S ribosomal RNA (rRNA) sequencing, shotgun metagenomics, metatranscriptomics, metaproteomics, and metabolomics. It highlighted their principles, diagnostic capabilities, and limitations in analyzing microbial communities in caries, endodontic infections, and periodontitis. It also reviewed auxiliary tools such as quantitative polymerase chain reaction (qPCR), microarrays, fluorescence in situ hybridization (FISH), and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS), and discussed the integration of artificial intelligence (AI) in metagenomic data interpretation.
RESULTS: Metagenomic studies have expanded the scope of known microbial species involved in dental caries beyond Streptococcus mutans, highlighting the contributions of Lactobacillus, Veillonella, Actinomyces, and Candida albicans. In endodontics, resistant species such as Enterococcus faecalis, Porphyromonas endodontalis, and Fusobacterium nucleatum are implicated in persistent infections. In periodontitis, a dysbiotic microbial shift has been associated with the presence of complex microbial consortia, including red and orange complex bacteria.
CONCLUSION: Metagenomics is a powerful diagnostic tool that provides an in-depth characterization of the complex microbial ecosystem of the oral cavity. It offers diagnostic potential through early and accurate detection of pathogenic shifts, promotes personalized treatment planning, and opens avenues for the development of potential biomarkers of disease progression.
CLINICAL SIGNIFICANCE: The integration of metagenomics into dental practice can revolutionize caries risk assessment, treatment precision, and disease prevention strategies. Although challenges such as high cost, data complexity, and lack of standardization remain, ongoing advancements in sequencing technologies and bioinformatics are expected to enhance its accessibility and clinical relevance.
HOW TO CITE THIS ARTICLE: Walia T, Srivastava N, Shetty RM, et al. Metagenomics as an Effective Diagnostic Approach for Exploring Oral Microbial Diversity and Dental Diseases: A Narrative Review. Int J Clin Pediatr Dent 2026;19(2):278-284.
Additional Links: PMID-41800013
PubMed:
Citation:
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@article {pmid41800013,
year = {2026},
author = {Walia, T and Srivastava, N and Shetty, RM and Rana, V},
title = {Metagenomics as an Effective Diagnostic Approach for Exploring Oral Microbial Diversity and Dental Diseases: A Narrative Review.},
journal = {International journal of clinical pediatric dentistry},
volume = {19},
number = {2},
pages = {278-284},
pmid = {41800013},
issn = {0974-7052},
abstract = {AIM AND BACKGROUND: The oral cavity harbors a diverse microbiota that significantly influences oral health and disease. Conventional microbiological techniques have limitations in detecting the full range of microbial species, particularly those that are uncultivable. Metagenomics, through culture-independent, high-throughput sequencing methods, offers a comprehensive approach to studying oral microbial diversity. This narrative review aims to evaluate the role of metagenomics in exploring the oral microbiome and its association with dental diseases.
METHODS: This review systematically synthesized current literature and research on metagenomic technologies, including 16S ribosomal RNA (rRNA) sequencing, shotgun metagenomics, metatranscriptomics, metaproteomics, and metabolomics. It highlighted their principles, diagnostic capabilities, and limitations in analyzing microbial communities in caries, endodontic infections, and periodontitis. It also reviewed auxiliary tools such as quantitative polymerase chain reaction (qPCR), microarrays, fluorescence in situ hybridization (FISH), and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS), and discussed the integration of artificial intelligence (AI) in metagenomic data interpretation.
RESULTS: Metagenomic studies have expanded the scope of known microbial species involved in dental caries beyond Streptococcus mutans, highlighting the contributions of Lactobacillus, Veillonella, Actinomyces, and Candida albicans. In endodontics, resistant species such as Enterococcus faecalis, Porphyromonas endodontalis, and Fusobacterium nucleatum are implicated in persistent infections. In periodontitis, a dysbiotic microbial shift has been associated with the presence of complex microbial consortia, including red and orange complex bacteria.
CONCLUSION: Metagenomics is a powerful diagnostic tool that provides an in-depth characterization of the complex microbial ecosystem of the oral cavity. It offers diagnostic potential through early and accurate detection of pathogenic shifts, promotes personalized treatment planning, and opens avenues for the development of potential biomarkers of disease progression.
CLINICAL SIGNIFICANCE: The integration of metagenomics into dental practice can revolutionize caries risk assessment, treatment precision, and disease prevention strategies. Although challenges such as high cost, data complexity, and lack of standardization remain, ongoing advancements in sequencing technologies and bioinformatics are expected to enhance its accessibility and clinical relevance.
HOW TO CITE THIS ARTICLE: Walia T, Srivastava N, Shetty RM, et al. Metagenomics as an Effective Diagnostic Approach for Exploring Oral Microbial Diversity and Dental Diseases: A Narrative Review. Int J Clin Pediatr Dent 2026;19(2):278-284.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Evaluation of Agolin® Pig on sow and piglet performance and sow fecal microbial communities during lactation.
Translational animal science, 10:txag023.
Essential oils are increasingly evaluated as alternatives to antibiotics in swine nutrition. This pilot study investigated the effects of Agolin Pig, a blend of microencapsulated essential oils, on sow performance, piglet growth, and sow fecal microbiota during lactation. Twenty-five sows were randomly assigned to either a control group (CON; n = 13) or a treatment group supplemented with Agolin Pig (AGO; n = 12; 200 ppm) from two weeks pre-farrowing through lactation. Diets for both groups met NRC (2012) nutrient requirements. Sow average daily feed intake (ADFI), body weight, body condition score (BCS), and Knauer Caliper measurements were collected at baseline, one week post-farrowing, and weaning. Piglet average daily gain (ADG) was recorded throughout lactation. Sow fecal samples were collected on d-14, d-7, d0, d8, and d16 relative to farrowing for microbiome analysis. Performance data were analyzed using PROC GLM or MIXED (SAS 9.4), with parity, number nursed, number weaned, and lactation week included as covariates. Microbiota data were analyzed in QIIME2 (v2022.8) and R (v4.2.3). Agolin Pig supplementation did not affect sow ADFI, piglet ADG, or colostrum and milk composition. However, AGO sows lost significantly less body condition during lactation, as measured by the Knauer Caliper (P = 0.010). Beta diversity differed between treatments on d8 (P = 0.029) and tended to differ on d16 (P = 0.066). Additionally, Clostridium and Streptococcus increased in CON but not AGO sows on d8 and d16, respectively. In summary, Agolin Pig supplementation reduced body condition loss and altered sow fecal microbiota diversity during lactation. These findings highlight the potential of essential oils to support sow health and productivity and warrant confirmation in larger studies.
Additional Links: PMID-41799843
PubMed:
Citation:
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@article {pmid41799843,
year = {2026},
author = {Fisk, AE and Dong, WX and Johnson, TA and Harlow, K and Scaff, TJ and DeDecker, AE and Hoogland, MJ and Parsley, MA and Richert, BT and Stewart, KR},
title = {Evaluation of Agolin® Pig on sow and piglet performance and sow fecal microbial communities during lactation.},
journal = {Translational animal science},
volume = {10},
number = {},
pages = {txag023},
pmid = {41799843},
issn = {2573-2102},
abstract = {Essential oils are increasingly evaluated as alternatives to antibiotics in swine nutrition. This pilot study investigated the effects of Agolin Pig, a blend of microencapsulated essential oils, on sow performance, piglet growth, and sow fecal microbiota during lactation. Twenty-five sows were randomly assigned to either a control group (CON; n = 13) or a treatment group supplemented with Agolin Pig (AGO; n = 12; 200 ppm) from two weeks pre-farrowing through lactation. Diets for both groups met NRC (2012) nutrient requirements. Sow average daily feed intake (ADFI), body weight, body condition score (BCS), and Knauer Caliper measurements were collected at baseline, one week post-farrowing, and weaning. Piglet average daily gain (ADG) was recorded throughout lactation. Sow fecal samples were collected on d-14, d-7, d0, d8, and d16 relative to farrowing for microbiome analysis. Performance data were analyzed using PROC GLM or MIXED (SAS 9.4), with parity, number nursed, number weaned, and lactation week included as covariates. Microbiota data were analyzed in QIIME2 (v2022.8) and R (v4.2.3). Agolin Pig supplementation did not affect sow ADFI, piglet ADG, or colostrum and milk composition. However, AGO sows lost significantly less body condition during lactation, as measured by the Knauer Caliper (P = 0.010). Beta diversity differed between treatments on d8 (P = 0.029) and tended to differ on d16 (P = 0.066). Additionally, Clostridium and Streptococcus increased in CON but not AGO sows on d8 and d16, respectively. In summary, Agolin Pig supplementation reduced body condition loss and altered sow fecal microbiota diversity during lactation. These findings highlight the potential of essential oils to support sow health and productivity and warrant confirmation in larger studies.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Gut microbiota and metabolic characteristics in subthreshold depression based on multi-omics.
Frontiers in psychiatry, 17:1760479.
BACKGROUND: Subthreshold depression (SD) is an intermediate state between normal mood and major depressive disorder (MDD), but its biological underpinnings remain insufficiently understood. Increasing evidence suggests that gut microbiota and host metabolic alterations may contribute to early depressive pathophysiology.
METHODS: We performed full-length 16S rRNA gene sequencing and LC-MS-based untargeted metabolomics on stool and plasma samples obtained from SD subjects and healthy controls. Microbial diversity, taxonomic composition, metabolic pathway alterations, and gut microbiota-metabolite associations were analyzed using bioinformatics pipelines, KEGG annotation, and Spearman correlation analysis.
RESULTS: SD patients exhibited marked gut microbial disturbances, including reduced microbial diversity and altered abundances of key genera such as decreased Eubacterium hallii group, Blautia, Dorea, and Agathobacter, and increased Escherichia-Shigella, Monoglobus, and Lachnoclostridium. Metabolomic profiling identified widespread metabolic perturbations, mainly affecting lipid metabolism, steroid hormone biosynthesis, and amino acid pathways. Exploratory correlation analysis indicated that beneficial taxa (e.g., Eubacterium hallii group and Blautia) were positively associated with specific glycerophospholipid and steroid hormone metabolites, whereas inverse associations were observed for other lipid-related metabolites.
CONCLUSION: This integrative microbiome-metabolome analysis demonstrates that SD is accompanied by early disruptions in gut microbial composition and systemic metabolism, particularly within lipid-related pathways. These findings suggest that gut microbiota dysbiosis may reflect early metabolic dysregulation and depression-related biological vulnerability in SD and highlight the gut microbiota as a candidate biological target for early identification and intervention.
Additional Links: PMID-41799813
PubMed:
Citation:
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@article {pmid41799813,
year = {2026},
author = {Xian, J and Wang, L and Shang, R and Sun, M and Yua, HJ and Zhang, X and Cheng, B and Wang, SJ and Tan, QW},
title = {Gut microbiota and metabolic characteristics in subthreshold depression based on multi-omics.},
journal = {Frontiers in psychiatry},
volume = {17},
number = {},
pages = {1760479},
pmid = {41799813},
issn = {1664-0640},
abstract = {BACKGROUND: Subthreshold depression (SD) is an intermediate state between normal mood and major depressive disorder (MDD), but its biological underpinnings remain insufficiently understood. Increasing evidence suggests that gut microbiota and host metabolic alterations may contribute to early depressive pathophysiology.
METHODS: We performed full-length 16S rRNA gene sequencing and LC-MS-based untargeted metabolomics on stool and plasma samples obtained from SD subjects and healthy controls. Microbial diversity, taxonomic composition, metabolic pathway alterations, and gut microbiota-metabolite associations were analyzed using bioinformatics pipelines, KEGG annotation, and Spearman correlation analysis.
RESULTS: SD patients exhibited marked gut microbial disturbances, including reduced microbial diversity and altered abundances of key genera such as decreased Eubacterium hallii group, Blautia, Dorea, and Agathobacter, and increased Escherichia-Shigella, Monoglobus, and Lachnoclostridium. Metabolomic profiling identified widespread metabolic perturbations, mainly affecting lipid metabolism, steroid hormone biosynthesis, and amino acid pathways. Exploratory correlation analysis indicated that beneficial taxa (e.g., Eubacterium hallii group and Blautia) were positively associated with specific glycerophospholipid and steroid hormone metabolites, whereas inverse associations were observed for other lipid-related metabolites.
CONCLUSION: This integrative microbiome-metabolome analysis demonstrates that SD is accompanied by early disruptions in gut microbial composition and systemic metabolism, particularly within lipid-related pathways. These findings suggest that gut microbiota dysbiosis may reflect early metabolic dysregulation and depression-related biological vulnerability in SD and highlight the gut microbiota as a candidate biological target for early identification and intervention.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Periodontal disease and neuroinflammation in multiple sclerosis: a systematic review of current evidence.
Frontiers in dental medicine, 7:1701357.
BACKGROUND: Multiple Sclerosis (MS) is a chronic, immune-mediated neurological disorder characterized by demyelination and neurodegeneration. Emerging evidence suggests a link between MS and Periodontal Diseases (PD) through shared immune-inflammatory pathways. This review assesses the association between periodontal diseases and multiple sclerosis, focusing on immune-inflammatory interactions and clinical correlations. Despite emerging evidence, the strength of association remains unclear due to methodological heterogeneity.
AIM: To review and evaluate the literature on the epidemiological association between PD and MS in adults.
MATERIALS AND METHODS: A systematic search was conducted in PubMed, Scopus, and Cochrane. Studies with full text articles that are available in English, without time restrictions, that assessed periodontitis, oral microbiome, and salivary biomarkers in relation to MS were included. Observational studies evaluating clinical, microbiological, or immunological associations were selected. Data extraction covered periodontal parameters, salivary biomarkers, periodontal pathogens and disease severity. The risk of bias was evaluated using Newcastle-Ottawa Scale.
RESULTS: The findings indicated that patients with MS had poorer periodontal health, when compared to healthy controls. Dysbiosis in the oral microbiome was observed, with a higher abundance of periodontal pathogens. Patients with MS exhibited elevated neutrophil-lymphocyte ratios and total oxidative stress, indicating a potential link between systemic inflammation and periodontal dysbiosis. While some studies established positive association between PD and MS, others highlighted the need for further investigation due to inconsistent findings in periodontal parameters between MS patients and controls.
CONCLUSION: Despite methodological heterogeneity, the available limited evidence indicates the association between periodontitis and MS. This highlights the need for standardized periodontal assessments in research involving MS and suggests that periodontal care may hold potential as an adjunct in management of MS.
Additional Links: PMID-41799794
PubMed:
Citation:
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@article {pmid41799794,
year = {2026},
author = {Santhanakrishnan, S and Kannappan, K and Krithika, C and Sridhar, C and Mahendra, J},
title = {Periodontal disease and neuroinflammation in multiple sclerosis: a systematic review of current evidence.},
journal = {Frontiers in dental medicine},
volume = {7},
number = {},
pages = {1701357},
pmid = {41799794},
issn = {2673-4915},
abstract = {BACKGROUND: Multiple Sclerosis (MS) is a chronic, immune-mediated neurological disorder characterized by demyelination and neurodegeneration. Emerging evidence suggests a link between MS and Periodontal Diseases (PD) through shared immune-inflammatory pathways. This review assesses the association between periodontal diseases and multiple sclerosis, focusing on immune-inflammatory interactions and clinical correlations. Despite emerging evidence, the strength of association remains unclear due to methodological heterogeneity.
AIM: To review and evaluate the literature on the epidemiological association between PD and MS in adults.
MATERIALS AND METHODS: A systematic search was conducted in PubMed, Scopus, and Cochrane. Studies with full text articles that are available in English, without time restrictions, that assessed periodontitis, oral microbiome, and salivary biomarkers in relation to MS were included. Observational studies evaluating clinical, microbiological, or immunological associations were selected. Data extraction covered periodontal parameters, salivary biomarkers, periodontal pathogens and disease severity. The risk of bias was evaluated using Newcastle-Ottawa Scale.
RESULTS: The findings indicated that patients with MS had poorer periodontal health, when compared to healthy controls. Dysbiosis in the oral microbiome was observed, with a higher abundance of periodontal pathogens. Patients with MS exhibited elevated neutrophil-lymphocyte ratios and total oxidative stress, indicating a potential link between systemic inflammation and periodontal dysbiosis. While some studies established positive association between PD and MS, others highlighted the need for further investigation due to inconsistent findings in periodontal parameters between MS patients and controls.
CONCLUSION: Despite methodological heterogeneity, the available limited evidence indicates the association between periodontitis and MS. This highlights the need for standardized periodontal assessments in research involving MS and suggests that periodontal care may hold potential as an adjunct in management of MS.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Gut Microbiota Signatures and Potential Mediators in the Trajectory of Age-related Macular Degeneration: A Phased Atlas by Genetic Inference.
International journal of medical sciences, 23(3):950-962.
PURPOSE: To depict an atlas of stage-stratified gut microbiota (GM) signatures and intermediatory metabolites, inflammatory proteins, and immune cell traits, governing the AMD trajectory.
METHODS: We deployed bidirectional two-sample Mendelian randomization (TSMR) integrating GWAS data of 207 GM taxa from the Dutch Microbiome Project (N = 7,738), and multiple AMD stages/subtypes, including 'Macular degeneration (senile) of retina', 'Early AMD', 'Disease progression to GA/CNV', 'Dry AMD includes GA', and 'Wet AMD', encapsulating the disease trajectory (N > 410,000), complemented by multivariable MR (MVMR) mediation analysis of 1,400 circulating metabolites, 731 immune cell traits, and 91 inflammatory proteins.
RESULTS: We identified 12/8/5/2/9/8 genetically predicted causal GM taxa of various AMD stages/subtypes as a stage-stratified GM signature across the AMD trajectory, among which g.Ruminococcaceae and s.Ruminococcaceae_bacterium_D16 were the sole shared GM taxa in triple AMD stages, while s.Bacteroides eggerthii, c.Gammaproteobacteria, s.Dorea and s.Ruminococcus_obeum influence dual AMD stages. Bidirectional analysis revealed that f.Streptococcaceae, g.Erysipelotrichaceae_noname, g.Streptococcus, s.Streptococcus_thermophilus, g.Ruminococcaceae_noname, and s.Ruminococcaceae_bacterium_D16 exhibited genetically reciprocal causation with AMD. We also proposed that Firmicutes may exhibit stage-specific duality depending on their constituent members and AMD stages. Several understudied GM from p.Actinobacteria and p.Verrucomicrobia have been implicated as AMD-associated taxa for the first time. Key metabolites, immune cell traits, and inflammatory proteins were established as significant mediators of GM-AMD links.
CONCLUSIONS: This first phased atlas uncovers GM effects over the AMD course, identifying potential microbial and biochemical targets for intervening in disease development.
Additional Links: PMID-41799763
PubMed:
Citation:
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@article {pmid41799763,
year = {2026},
author = {Zhou, Y and Wang, Z and Huang, C and Yu, X and Chen, J and Jiang, X and Dong, J and Peng, Q and Li, L and Song, X and Lu, X},
title = {Gut Microbiota Signatures and Potential Mediators in the Trajectory of Age-related Macular Degeneration: A Phased Atlas by Genetic Inference.},
journal = {International journal of medical sciences},
volume = {23},
number = {3},
pages = {950-962},
pmid = {41799763},
issn = {1449-1907},
mesh = {Humans ; *Gastrointestinal Microbiome/genetics/immunology ; *Macular Degeneration/genetics/microbiology/immunology/pathology ; Mendelian Randomization Analysis ; Genome-Wide Association Study ; Disease Progression ; Polymorphism, Single Nucleotide ; },
abstract = {PURPOSE: To depict an atlas of stage-stratified gut microbiota (GM) signatures and intermediatory metabolites, inflammatory proteins, and immune cell traits, governing the AMD trajectory.
METHODS: We deployed bidirectional two-sample Mendelian randomization (TSMR) integrating GWAS data of 207 GM taxa from the Dutch Microbiome Project (N = 7,738), and multiple AMD stages/subtypes, including 'Macular degeneration (senile) of retina', 'Early AMD', 'Disease progression to GA/CNV', 'Dry AMD includes GA', and 'Wet AMD', encapsulating the disease trajectory (N > 410,000), complemented by multivariable MR (MVMR) mediation analysis of 1,400 circulating metabolites, 731 immune cell traits, and 91 inflammatory proteins.
RESULTS: We identified 12/8/5/2/9/8 genetically predicted causal GM taxa of various AMD stages/subtypes as a stage-stratified GM signature across the AMD trajectory, among which g.Ruminococcaceae and s.Ruminococcaceae_bacterium_D16 were the sole shared GM taxa in triple AMD stages, while s.Bacteroides eggerthii, c.Gammaproteobacteria, s.Dorea and s.Ruminococcus_obeum influence dual AMD stages. Bidirectional analysis revealed that f.Streptococcaceae, g.Erysipelotrichaceae_noname, g.Streptococcus, s.Streptococcus_thermophilus, g.Ruminococcaceae_noname, and s.Ruminococcaceae_bacterium_D16 exhibited genetically reciprocal causation with AMD. We also proposed that Firmicutes may exhibit stage-specific duality depending on their constituent members and AMD stages. Several understudied GM from p.Actinobacteria and p.Verrucomicrobia have been implicated as AMD-associated taxa for the first time. Key metabolites, immune cell traits, and inflammatory proteins were established as significant mediators of GM-AMD links.
CONCLUSIONS: This first phased atlas uncovers GM effects over the AMD course, identifying potential microbial and biochemical targets for intervening in disease development.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome/genetics/immunology
*Macular Degeneration/genetics/microbiology/immunology/pathology
Mendelian Randomization Analysis
Genome-Wide Association Study
Disease Progression
Polymorphism, Single Nucleotide
RevDate: 2026-03-09
CmpDate: 2026-03-09
Human milk oligosaccharides promote synaptogenesis and neurite outgrowth in human cortical organoids.
Biochemistry and biophysics reports, 45:102529.
The first 1000 days of a child's life represent a critical window for brain development, during which nutrition exerts profound effects on the trajectories of neurodevelopment. Human Milk Oligosaccharides (HMOs), a major component of human milk, are largely indigestible by infants and are known to influence immunity, microbiome composition, and gut-brain signaling, but their direct role in neurodevelopment remains poorly understood. Here, we investigated the impact of HMOs on human cortical organoids, a physiologically relevant in vitro model of early brain development. We found that HMO treatment significantly enhanced neurite outgrowth and synaptogenesis in a dose-dependent manner. Global proteomic profiling further demonstrated the upregulation of proteins associated with neuronal differentiation, synaptic maturation, and cytoskeletal remodeling. Our findings suggest that HMOs can influence neurodevelopmental processes and highlight a potential role for maternal milk components in early brain development.
Additional Links: PMID-41799697
PubMed:
Citation:
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@article {pmid41799697,
year = {2026},
author = {Bulcão V C, L and Moreira, NCS and Carvalho, PC and Luz, IS and de S da G Fischer, J and Tsu, BL and Sejane, K and Savo, C and Martins, AMA and Bode, L and Muotri, AR},
title = {Human milk oligosaccharides promote synaptogenesis and neurite outgrowth in human cortical organoids.},
journal = {Biochemistry and biophysics reports},
volume = {45},
number = {},
pages = {102529},
pmid = {41799697},
issn = {2405-5808},
abstract = {The first 1000 days of a child's life represent a critical window for brain development, during which nutrition exerts profound effects on the trajectories of neurodevelopment. Human Milk Oligosaccharides (HMOs), a major component of human milk, are largely indigestible by infants and are known to influence immunity, microbiome composition, and gut-brain signaling, but their direct role in neurodevelopment remains poorly understood. Here, we investigated the impact of HMOs on human cortical organoids, a physiologically relevant in vitro model of early brain development. We found that HMO treatment significantly enhanced neurite outgrowth and synaptogenesis in a dose-dependent manner. Global proteomic profiling further demonstrated the upregulation of proteins associated with neuronal differentiation, synaptic maturation, and cytoskeletal remodeling. Our findings suggest that HMOs can influence neurodevelopmental processes and highlight a potential role for maternal milk components in early brain development.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
The Role of the Gut Microbiome in Clinical Outcomes of Colorectal Cancer: A Systematic Review (2020-2025).
Oncology research, 34(3):3.
BACKGROUND: The Colorectal Cancer (CRC) pathogenesis and therapeutic efficacy are influenced by the gut microbiome, making it a promising biomarker for predicting treatment responses and adverse effects. This systematic review aims to outline the gut microbiome composition in individuals with CRC undergoing the same therapeutic regimen and evaluate interindividual microbiome profile variations to better understand how these differences may influence therapeutic outcomes.
METHODS: Key studies investigating the microbiome's role in therapeutic approaches for CRC were searched in both PubMed and Cochrane databases on 12 and 22 March 2025, respectively. Eligible studies included free full-text English-language randomized clinical trials and human observational studies reporting on gut microbiome composition and treatment outcomes. RoB 2 and ROBINS-I were employed in the evaluation of bias for randomized trials and observational studies, respectively. Data extracted was narratively analyzed.
RESULTS: Six studies involving a total of 361 individuals were included. Therapeutic interventions, either standard treatments and/or those targeting the gut microbiome, generally increased probiotic taxa and reduced pro-carcinogenic bacteria. However, no consistent pattern of improved clinical outcomes was observed, suggesting that treatment mechanisms, the tumor's nature, and individual characteristics play critical roles in microbiome modulation.
CONCLUSION: The gut microbiome holds significant potential in clinical settings. Nonetheless, further research is needed to better understand its functional aspects and to consider the influence of treatment mechanisms, the tumor's nature, and individual characteristics as modulators, in order to optimize clinical outcomes.
Additional Links: PMID-41799504
PubMed:
Citation:
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@article {pmid41799504,
year = {2026},
author = {Santos, I and Liberal, J and Teixeira, P and Martins, D and Mendes, F},
title = {The Role of the Gut Microbiome in Clinical Outcomes of Colorectal Cancer: A Systematic Review (2020-2025).},
journal = {Oncology research},
volume = {34},
number = {3},
pages = {3},
pmid = {41799504},
issn = {1555-3906},
mesh = {Humans ; *Colorectal Neoplasms/microbiology/therapy ; *Gastrointestinal Microbiome ; Treatment Outcome ; Probiotics/therapeutic use ; Randomized Controlled Trials as Topic ; },
abstract = {BACKGROUND: The Colorectal Cancer (CRC) pathogenesis and therapeutic efficacy are influenced by the gut microbiome, making it a promising biomarker for predicting treatment responses and adverse effects. This systematic review aims to outline the gut microbiome composition in individuals with CRC undergoing the same therapeutic regimen and evaluate interindividual microbiome profile variations to better understand how these differences may influence therapeutic outcomes.
METHODS: Key studies investigating the microbiome's role in therapeutic approaches for CRC were searched in both PubMed and Cochrane databases on 12 and 22 March 2025, respectively. Eligible studies included free full-text English-language randomized clinical trials and human observational studies reporting on gut microbiome composition and treatment outcomes. RoB 2 and ROBINS-I were employed in the evaluation of bias for randomized trials and observational studies, respectively. Data extracted was narratively analyzed.
RESULTS: Six studies involving a total of 361 individuals were included. Therapeutic interventions, either standard treatments and/or those targeting the gut microbiome, generally increased probiotic taxa and reduced pro-carcinogenic bacteria. However, no consistent pattern of improved clinical outcomes was observed, suggesting that treatment mechanisms, the tumor's nature, and individual characteristics play critical roles in microbiome modulation.
CONCLUSION: The gut microbiome holds significant potential in clinical settings. Nonetheless, further research is needed to better understand its functional aspects and to consider the influence of treatment mechanisms, the tumor's nature, and individual characteristics as modulators, in order to optimize clinical outcomes.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Colorectal Neoplasms/microbiology/therapy
*Gastrointestinal Microbiome
Treatment Outcome
Probiotics/therapeutic use
Randomized Controlled Trials as Topic
RevDate: 2026-03-09
CmpDate: 2026-03-09
Human Leukocyte Antigen Alleles and Oral Microbiome Association With Antibody-mediated Rejection in Living-donor Liver Transplant Patients.
Journal of clinical and experimental hepatology, 16(3):103494.
BACKGROUND/AIMS: Antibody-mediated rejection (ABMR) is an important cause of graft dysfunction after liver transplantation, yet the combined influence of human leukocyte antigen (HLA) immunogenetics and the oral microbiome on ABMR risk is not well defined.
METHODS: In this prospective cohort of 180 living donor-recipient pairs, pre-transplant 16S ribosomal ribonucleic acid sequences and high-resolution HLA genotyping were done. The human leukocyte antigen epitope mismatch algorithm quantified amino acid and solvent-accessible mismatches. Oral microbiome profiles were generated using the Divisive Amplicon Denoising Algorithm (DADA2) and quantitative insights into microbial ecology version 2 (QIIME2). Associations between HLA alleles and microbial taxa were assessed using generalized linear models and linear discriminant analysis effect size (LEfSe). ABMR was diagnosed as per Banff criteria over one year.
RESULTS: ABMR was diagnosed in 15 patients. These patients had significantly higher mismatch burdens at HLA-DPB1, DQB1, and DRB1 than non-ABMR recipients. Across the cohort, 68 HLA alleles demonstrated distinct microbial associations at phylum, family, and genus levels. Alleles such as HLA-DRB108, HLA-DPB1575, and HLA-C05 were linked to differential abundance of Actinobacteriota, Campylobacterota, and Fusobacteriota, respectively. Genus-level analyses revealed strong allele-specific associations with Veillonella, Enterobacter, Streptococcus, and other immunomodulatory taxa. LEfSe identified HLA-DQB106 and HLA-DQB1∗104 as associated with enrichment of Enterobacter, Citrobacter europaeus, Bacteroides plebeius, Rothia dentocariosa, Megasphaera, and Burkholderiaceae-microbial signatures also prominent in ABMR cases.
CONCLUSION: Class II HLA mismatch burden and allele-specific oral microbial signatures are closely linked to ABMR. Combined HLA-microbiome profiling may enhance early risk stratification and inform targeted peri-transplant microbial interventions.
Additional Links: PMID-41799378
PubMed:
Citation:
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@article {pmid41799378,
year = {2026},
author = {Kaur, M and Babu, R and Baweja, S and Gupta, R and Singh, SP and Pamecha, V and Bihari, C},
title = {Human Leukocyte Antigen Alleles and Oral Microbiome Association With Antibody-mediated Rejection in Living-donor Liver Transplant Patients.},
journal = {Journal of clinical and experimental hepatology},
volume = {16},
number = {3},
pages = {103494},
pmid = {41799378},
issn = {0973-6883},
abstract = {BACKGROUND/AIMS: Antibody-mediated rejection (ABMR) is an important cause of graft dysfunction after liver transplantation, yet the combined influence of human leukocyte antigen (HLA) immunogenetics and the oral microbiome on ABMR risk is not well defined.
METHODS: In this prospective cohort of 180 living donor-recipient pairs, pre-transplant 16S ribosomal ribonucleic acid sequences and high-resolution HLA genotyping were done. The human leukocyte antigen epitope mismatch algorithm quantified amino acid and solvent-accessible mismatches. Oral microbiome profiles were generated using the Divisive Amplicon Denoising Algorithm (DADA2) and quantitative insights into microbial ecology version 2 (QIIME2). Associations between HLA alleles and microbial taxa were assessed using generalized linear models and linear discriminant analysis effect size (LEfSe). ABMR was diagnosed as per Banff criteria over one year.
RESULTS: ABMR was diagnosed in 15 patients. These patients had significantly higher mismatch burdens at HLA-DPB1, DQB1, and DRB1 than non-ABMR recipients. Across the cohort, 68 HLA alleles demonstrated distinct microbial associations at phylum, family, and genus levels. Alleles such as HLA-DRB108, HLA-DPB1575, and HLA-C05 were linked to differential abundance of Actinobacteriota, Campylobacterota, and Fusobacteriota, respectively. Genus-level analyses revealed strong allele-specific associations with Veillonella, Enterobacter, Streptococcus, and other immunomodulatory taxa. LEfSe identified HLA-DQB106 and HLA-DQB1∗104 as associated with enrichment of Enterobacter, Citrobacter europaeus, Bacteroides plebeius, Rothia dentocariosa, Megasphaera, and Burkholderiaceae-microbial signatures also prominent in ABMR cases.
CONCLUSION: Class II HLA mismatch burden and allele-specific oral microbial signatures are closely linked to ABMR. Combined HLA-microbiome profiling may enhance early risk stratification and inform targeted peri-transplant microbial interventions.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Bacterial vesicles-initiated in-situ spray-polymerized coating enables synergistic antibacterial-photothermal functionality for accelerating wound healing.
Theranostics, 16(9):4566-4579.
BACKGROUND: Although microbial therapies can address the harm to beneficial bacteria and microbiome balance caused by traditional antibacterial treatments in skin damage and infection, their pathogenic potential limits clinical application. Bacterial extracellular vesicles (BEVs) offer a safer alternative by targeting microbes and modulating immunity.
METHODS: Lactobacillus reuteri-derived BEVs (LBEVs) are functionalized with Fe [3+] via electrostatic adsorption, and co-sprayed with pyrrole monomers onto wounds to initiate oxidative polymerization and then form conformal polypyrrole coatings (LBEVs-PPy). Thanks to the natural antibacterial activity of LBEVs, the LBEVs-PPy coating could inhibit the growth of pathogens efficiently. Furthermore, the mild hyperthermia induced by PPy's NIR-triggered photothermal activation significantly upregulates the expression of angiogenic regulators.
RESULTS: In vitro, LBEVs effectively inhibited the growth of S. aureus, E. coli, and S. epidermidis, demonstrating potent antibacterial efficacy. Following mild hyperthermia (42 °C for 1 h), HUVECs showed elevated expression of angiogenic regulators, including VEGFA and ANGPT1. This treatment also activates HSP90/p-eNOS pathway in HUVECs, thereby accelerating angiogenesis. In a mouse model of skin damage and infection, LBEVs-PPy coating significantly accelerates wound healing through synergistic mechanisms that integrate the antibacterial activity of LBEVs and the photothermal effect of PPy.
CONCLUSIONS: Our research developed an in-situ spray-polymerized coating integrating antibacterial and photothermal modalities, thus presenting a promising biotherapeutic platform for clinical wound management and tissue regeneration.
Additional Links: PMID-41799196
PubMed:
Citation:
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@article {pmid41799196,
year = {2026},
author = {Wang, D and Liang, S and Ai, Z and Kong, Q and Xing, D and Cao, Z and Geng, Z},
title = {Bacterial vesicles-initiated in-situ spray-polymerized coating enables synergistic antibacterial-photothermal functionality for accelerating wound healing.},
journal = {Theranostics},
volume = {16},
number = {9},
pages = {4566-4579},
pmid = {41799196},
issn = {1838-7640},
mesh = {Animals ; *Wound Healing/drug effects ; *Anti-Bacterial Agents/pharmacology ; Mice ; Humans ; *Extracellular Vesicles/chemistry/metabolism ; Escherichia coli/drug effects ; Human Umbilical Vein Endothelial Cells ; Polymers/chemistry/pharmacology ; *Photothermal Therapy/methods ; Staphylococcus aureus/drug effects ; Pyrroles/chemistry/pharmacology ; Disease Models, Animal ; Skin ; Neovascularization, Physiologic/drug effects ; Staphylococcus epidermidis/drug effects ; },
abstract = {BACKGROUND: Although microbial therapies can address the harm to beneficial bacteria and microbiome balance caused by traditional antibacterial treatments in skin damage and infection, their pathogenic potential limits clinical application. Bacterial extracellular vesicles (BEVs) offer a safer alternative by targeting microbes and modulating immunity.
METHODS: Lactobacillus reuteri-derived BEVs (LBEVs) are functionalized with Fe [3+] via electrostatic adsorption, and co-sprayed with pyrrole monomers onto wounds to initiate oxidative polymerization and then form conformal polypyrrole coatings (LBEVs-PPy). Thanks to the natural antibacterial activity of LBEVs, the LBEVs-PPy coating could inhibit the growth of pathogens efficiently. Furthermore, the mild hyperthermia induced by PPy's NIR-triggered photothermal activation significantly upregulates the expression of angiogenic regulators.
RESULTS: In vitro, LBEVs effectively inhibited the growth of S. aureus, E. coli, and S. epidermidis, demonstrating potent antibacterial efficacy. Following mild hyperthermia (42 °C for 1 h), HUVECs showed elevated expression of angiogenic regulators, including VEGFA and ANGPT1. This treatment also activates HSP90/p-eNOS pathway in HUVECs, thereby accelerating angiogenesis. In a mouse model of skin damage and infection, LBEVs-PPy coating significantly accelerates wound healing through synergistic mechanisms that integrate the antibacterial activity of LBEVs and the photothermal effect of PPy.
CONCLUSIONS: Our research developed an in-situ spray-polymerized coating integrating antibacterial and photothermal modalities, thus presenting a promising biotherapeutic platform for clinical wound management and tissue regeneration.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Wound Healing/drug effects
*Anti-Bacterial Agents/pharmacology
Mice
Humans
*Extracellular Vesicles/chemistry/metabolism
Escherichia coli/drug effects
Human Umbilical Vein Endothelial Cells
Polymers/chemistry/pharmacology
*Photothermal Therapy/methods
Staphylococcus aureus/drug effects
Pyrroles/chemistry/pharmacology
Disease Models, Animal
Skin
Neovascularization, Physiologic/drug effects
Staphylococcus epidermidis/drug effects
RevDate: 2026-03-09
CmpDate: 2026-03-09
Gut microbiome dysregulation is associated with segmental glomerulosclerosis in IgA nephropathy: insights from Oxford classification-based microbiome profiling.
Frontiers in cellular and infection microbiology, 16:1644626.
BACKGROUND: IgA nephropathy (IgAN) is a common immune-complex-mediated glomerulonephritis with segmental glomerulosclerosis (S lesion, S1 in Oxford classification) being an independent predictor of poor renal prognosis, where 20%-40% of IgAN-S1 patients progress to end-stage renal disease, but its pathogenesis is unclear.
METHODS: This study enrolled 12 IgAN-S0 (without segmental sclerosis) and 19 IgAN-S1 (with segmental sclerosis) patients, performed 16S rRNA gene sequencing on fecal samples, and analyzed gut microbiota composition and functions.
RESULTS: S1 had enriched Firmicutes and Patescibacteria while S0 had more Proteobacteria, Campylobacterota, and Desulfobacterota; LEfSe analysis identified Subdoligranulum and unclassified_Erysipelotrichaceae_UCG-003 as S1-specific biomarkers and Phascolarctobacterium, Streptococcus_parasanguinis, and Proteobacteria as S0 biomarkers (P<0.05). Functional prediction showed S1 was enriched in pro-inflammatory pathways like endoplasmic reticulum stress and secondary bile acid biosynthesis, while S0 had activated protective pathways such as cytochrome P450 drug metabolism and ubiquitin system.
CONCLUSIONS: This study reveals gut microbiota dysregulation is closely associated with IgAN segmental sclerosis, with S1 showing pro-inflammatory microbial profiles and S0 retaining protective functions, providing new insights into gut-kidney axis mechanisms and potential microbiome-targeted therapies for IgAN.
Additional Links: PMID-41798752
PubMed:
Citation:
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@article {pmid41798752,
year = {2026},
author = {Lu, B and Zhang, A and Wu, M and Chen, S and Wang, Y and Wang, J and Huang, M and Zhu, Y and Liu, H and Zhu, F and Zeng, X and Chen, S and Zhou, X and Lin, R},
title = {Gut microbiome dysregulation is associated with segmental glomerulosclerosis in IgA nephropathy: insights from Oxford classification-based microbiome profiling.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1644626},
pmid = {41798752},
issn = {2235-2988},
mesh = {Humans ; *Glomerulonephritis, IGA/microbiology/pathology ; *Gastrointestinal Microbiome ; Male ; RNA, Ribosomal, 16S/genetics ; Female ; Adult ; Feces/microbiology ; *Bacteria/classification/genetics/isolation & purification ; *Glomerulosclerosis, Focal Segmental/microbiology/pathology ; Middle Aged ; Biomarkers ; Dysbiosis ; DNA, Bacterial/genetics ; },
abstract = {BACKGROUND: IgA nephropathy (IgAN) is a common immune-complex-mediated glomerulonephritis with segmental glomerulosclerosis (S lesion, S1 in Oxford classification) being an independent predictor of poor renal prognosis, where 20%-40% of IgAN-S1 patients progress to end-stage renal disease, but its pathogenesis is unclear.
METHODS: This study enrolled 12 IgAN-S0 (without segmental sclerosis) and 19 IgAN-S1 (with segmental sclerosis) patients, performed 16S rRNA gene sequencing on fecal samples, and analyzed gut microbiota composition and functions.
RESULTS: S1 had enriched Firmicutes and Patescibacteria while S0 had more Proteobacteria, Campylobacterota, and Desulfobacterota; LEfSe analysis identified Subdoligranulum and unclassified_Erysipelotrichaceae_UCG-003 as S1-specific biomarkers and Phascolarctobacterium, Streptococcus_parasanguinis, and Proteobacteria as S0 biomarkers (P<0.05). Functional prediction showed S1 was enriched in pro-inflammatory pathways like endoplasmic reticulum stress and secondary bile acid biosynthesis, while S0 had activated protective pathways such as cytochrome P450 drug metabolism and ubiquitin system.
CONCLUSIONS: This study reveals gut microbiota dysregulation is closely associated with IgAN segmental sclerosis, with S1 showing pro-inflammatory microbial profiles and S0 retaining protective functions, providing new insights into gut-kidney axis mechanisms and potential microbiome-targeted therapies for IgAN.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Glomerulonephritis, IGA/microbiology/pathology
*Gastrointestinal Microbiome
Male
RNA, Ribosomal, 16S/genetics
Female
Adult
Feces/microbiology
*Bacteria/classification/genetics/isolation & purification
*Glomerulosclerosis, Focal Segmental/microbiology/pathology
Middle Aged
Biomarkers
Dysbiosis
DNA, Bacterial/genetics
RevDate: 2026-03-09
CmpDate: 2026-03-09
Predicting inter-microbial host specificity in oral biofilms using a lightweight relation-aware knowledge graph model.
Frontiers in cellular and infection microbiology, 16:1775191.
INTRODUCTION: The human oral cavity hosts a complex microbial ecosystem of bacteria, viruses, bacteriophages, and other microorganisms forming biofilms in different niches. Phage-bacteria host specificity is crucial in shaping microbial community, stability, and dysbiosis. mapping this specificity is limited by experimental constraints and traditional methods can't capture ecological complexity. The goal is to create a graph-based model that treats inter-microbial host specificity as a relational learning problem, integrating taxonomic, ecological, and infection data into a knowledge graph. This improves phage-bacteria host predictions and reveals microbial hubs and interaction patterns related to periodontal disease dysbiosis.
METHODS: This study introduces a lightweight, relation-aware knowledge graph for predicting microbial host specificity in oral biofilms. We built a heterogeneous graph of the oral microbiome, incorporating microbial taxa, anatomical sites, taxonomic hierarchies, enrichment patterns, and INFECTS relationships. The dataset includes 500 viral taxa across four oral niches, with 21,338 significant co-occurrence relationships and various biological features. To learn meaningful representations, we combined graph embeddings with microbial features. We developed a relation-aware graph neural network, IK-BRNet, to efficiently encode ecological and interaction semantics.
RESULTS: Model performance was evaluated against a conventional Graph Attention Network (GAT) using stratified training, validation, and test splits with class imbalance correction. IK-BRNet demonstrated faster convergence and superior discrimination ability, achieving a higher AUC-ROC (0.929 vs. 0.904) and markedly improved sensitivity for disease-associated viral taxa (93.8% vs. 56.3%). While the baseline GAT achieved higher accuracy and specificity, IK-BRNet consistently reduced false negatives, thereby improving its ability to detect disease-related microbial signals. Site-specific predictions confirmed biological validity, with the highest disease scores for dental plaque-associated viruses and lower scores in healthy niches such as the tongue and buccal mucosa.
CONCLSUION: This study shows that relation-aware graph learning offers a meaningful and efficient way to model inter-microbial host specificity in oral biofilms. The framework improves oral microbiome network inference and supports disease screening, ecological analysis, and microbiome-based dentistry.
Additional Links: PMID-41798747
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@article {pmid41798747,
year = {2026},
author = {Natarajan, PM and Varma, SR and Kodangattil Narayanan, J and Odeh, R},
title = {Predicting inter-microbial host specificity in oral biofilms using a lightweight relation-aware knowledge graph model.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1775191},
pmid = {41798747},
issn = {2235-2988},
mesh = {*Mouth/microbiology/virology ; *Biofilms/growth & development ; Humans ; Microbiota ; *Bacteria/classification ; *Host Specificity ; Neural Networks, Computer ; Bacteriophages/physiology ; Periodontal Diseases/microbiology ; Dysbiosis/microbiology ; },
abstract = {INTRODUCTION: The human oral cavity hosts a complex microbial ecosystem of bacteria, viruses, bacteriophages, and other microorganisms forming biofilms in different niches. Phage-bacteria host specificity is crucial in shaping microbial community, stability, and dysbiosis. mapping this specificity is limited by experimental constraints and traditional methods can't capture ecological complexity. The goal is to create a graph-based model that treats inter-microbial host specificity as a relational learning problem, integrating taxonomic, ecological, and infection data into a knowledge graph. This improves phage-bacteria host predictions and reveals microbial hubs and interaction patterns related to periodontal disease dysbiosis.
METHODS: This study introduces a lightweight, relation-aware knowledge graph for predicting microbial host specificity in oral biofilms. We built a heterogeneous graph of the oral microbiome, incorporating microbial taxa, anatomical sites, taxonomic hierarchies, enrichment patterns, and INFECTS relationships. The dataset includes 500 viral taxa across four oral niches, with 21,338 significant co-occurrence relationships and various biological features. To learn meaningful representations, we combined graph embeddings with microbial features. We developed a relation-aware graph neural network, IK-BRNet, to efficiently encode ecological and interaction semantics.
RESULTS: Model performance was evaluated against a conventional Graph Attention Network (GAT) using stratified training, validation, and test splits with class imbalance correction. IK-BRNet demonstrated faster convergence and superior discrimination ability, achieving a higher AUC-ROC (0.929 vs. 0.904) and markedly improved sensitivity for disease-associated viral taxa (93.8% vs. 56.3%). While the baseline GAT achieved higher accuracy and specificity, IK-BRNet consistently reduced false negatives, thereby improving its ability to detect disease-related microbial signals. Site-specific predictions confirmed biological validity, with the highest disease scores for dental plaque-associated viruses and lower scores in healthy niches such as the tongue and buccal mucosa.
CONCLSUION: This study shows that relation-aware graph learning offers a meaningful and efficient way to model inter-microbial host specificity in oral biofilms. The framework improves oral microbiome network inference and supports disease screening, ecological analysis, and microbiome-based dentistry.},
}
MeSH Terms:
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*Mouth/microbiology/virology
*Biofilms/growth & development
Humans
Microbiota
*Bacteria/classification
*Host Specificity
Neural Networks, Computer
Bacteriophages/physiology
Periodontal Diseases/microbiology
Dysbiosis/microbiology
RevDate: 2026-03-09
CmpDate: 2026-03-09
Diabetes Mellitus Accelerates Alzheimer's Disease Development by Affecting the Gut Microbiome.
BioMed research international, 2026:9974079.
Increasing evidence suggests a link between Alzheimer's disease (AD) and diabetes mellitus (DM). However, the precise mechanisms by which DM contributes to AD remain unclear. This study is aimed at elucidating the potential role of DM in the early stages of AD. Accordingly, a streptozotocin (STZ)-induced diabetic 5 × familial AD (FAD) mouse model was established. Immunohistochemistry and positron emission tomography/computed tomography (PET/CT) scanning were performed to examine amyloid beta (Aβ) deposition in the brain. The integrity of the colonic epithelium was assessed using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and immunofluorescence staining. Microbial diversity analysis was conducted for 5 × FAD mice with and without STZ-induced DM to determine shifts in intestinal flora profiles. After oral administration of butyrate to STZ-treated 5 × FAD mice, we observed that Aβ deposition in the brain was decreased, and the intestinal flora improved. Immunohistochemistry and PET/CT findings revealed a marked increase in Aβ formation in the brains of 5 × FAD mice treated with STZ. qRT-PCR and immunofluorescence staining revealed severe intestinal barrier dysfunction in these mice. Gut microbiota sequencing indicated significant dysbiosis in STZ-treated 5 × FAD mice, characterized by a reduction in short-chain fatty acid (SCFA)-producing species. After oral administration of butyrate, Aβ deposition in the brains of STZ-treated 5 × FAD mice was significantly reduced, and beneficial changes occurred in the intestinal flora, including increases in bacteria associated with SCFA production and neurological function. Dysregulation of the gut microbiome may exacerbate cerebral amyloidosis during AD pathogenesis. Microbes associated with SCFA production may play a beneficial role in AD treatment, and butyrate supplementation can significantly delay AD progression.
Additional Links: PMID-41798687
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@article {pmid41798687,
year = {2026},
author = {He, Q and Zhao, Z and Jiang, D and Fei, A},
title = {Diabetes Mellitus Accelerates Alzheimer's Disease Development by Affecting the Gut Microbiome.},
journal = {BioMed research international},
volume = {2026},
number = {},
pages = {9974079},
pmid = {41798687},
issn = {2314-6141},
mesh = {*Gastrointestinal Microbiome/physiology/drug effects ; *Alzheimer Disease/microbiology/pathology/metabolism ; Animals ; Mice ; Brain/metabolism/pathology/diagnostic imaging ; Amyloid beta-Peptides/metabolism ; *Diabetes Mellitus, Experimental/microbiology/complications ; Male ; Butyrates/pharmacology ; Disease Models, Animal ; Positron Emission Tomography Computed Tomography ; Mice, Inbred C57BL ; Fatty Acids, Volatile/metabolism ; },
abstract = {Increasing evidence suggests a link between Alzheimer's disease (AD) and diabetes mellitus (DM). However, the precise mechanisms by which DM contributes to AD remain unclear. This study is aimed at elucidating the potential role of DM in the early stages of AD. Accordingly, a streptozotocin (STZ)-induced diabetic 5 × familial AD (FAD) mouse model was established. Immunohistochemistry and positron emission tomography/computed tomography (PET/CT) scanning were performed to examine amyloid beta (Aβ) deposition in the brain. The integrity of the colonic epithelium was assessed using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and immunofluorescence staining. Microbial diversity analysis was conducted for 5 × FAD mice with and without STZ-induced DM to determine shifts in intestinal flora profiles. After oral administration of butyrate to STZ-treated 5 × FAD mice, we observed that Aβ deposition in the brain was decreased, and the intestinal flora improved. Immunohistochemistry and PET/CT findings revealed a marked increase in Aβ formation in the brains of 5 × FAD mice treated with STZ. qRT-PCR and immunofluorescence staining revealed severe intestinal barrier dysfunction in these mice. Gut microbiota sequencing indicated significant dysbiosis in STZ-treated 5 × FAD mice, characterized by a reduction in short-chain fatty acid (SCFA)-producing species. After oral administration of butyrate, Aβ deposition in the brains of STZ-treated 5 × FAD mice was significantly reduced, and beneficial changes occurred in the intestinal flora, including increases in bacteria associated with SCFA production and neurological function. Dysregulation of the gut microbiome may exacerbate cerebral amyloidosis during AD pathogenesis. Microbes associated with SCFA production may play a beneficial role in AD treatment, and butyrate supplementation can significantly delay AD progression.},
}
MeSH Terms:
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*Gastrointestinal Microbiome/physiology/drug effects
*Alzheimer Disease/microbiology/pathology/metabolism
Animals
Mice
Brain/metabolism/pathology/diagnostic imaging
Amyloid beta-Peptides/metabolism
*Diabetes Mellitus, Experimental/microbiology/complications
Male
Butyrates/pharmacology
Disease Models, Animal
Positron Emission Tomography Computed Tomography
Mice, Inbred C57BL
Fatty Acids, Volatile/metabolism
RevDate: 2026-03-09
CmpDate: 2026-03-09
Fecal microbiota transplantation in ulcerative colitis: evidence, mechanisms, and practice considerations.
Therapeutic advances in gastroenterology, 19:17562848261426284.
Ulcerative colitis (UC) is a chronic inflammatory bowel disease strongly associated with intestinal dysbiosis, reduced microbial diversity, and disrupted microbial metabolite profiles. Fecal microbiota transplantation (FMT) aims to restore microbial homeostasis and has shown a signal of benefit for induction of remission in some trials, but results are heterogeneous and long-term maintenance efficacy remains uncertain. In this narrative review, we synthesize randomized controlled trials (RCTs), systematic reviews/meta-analyses, and recent guideline and regulatory updates on FMT in UC, and integrate mechanistic insights from microbiome and metabolomics research. Across RCTs, intensive lower-gastrointestinal regimens using pooled, multidonor material, and/or anaerobic processing have most consistently achieved modestly higher steroid-free clinical and endoscopic remission than placebo in mild-to-moderate UC (approximately 25%-32% vs 5%-10% in representative studies), whereas upper-gastrointestinal delivery or oral lyophilized formulations and highly restrictive donor selection have yielded mixed or negative results. Mechanistically, responders commonly demonstrate engraftment of short-chain fatty acid producing taxa and restoration of secondary bile acid pathways. Safety profiles in trials are generally comparable to placebo for common mild adverse events, but rare severe transmissions (e.g., multidrug-resistant Escherichia coli and SARS-CoV-2) have driven stricter donor screening and have limited routine use outside regulated programs. Current guidelines recommend against FMT for UC outside clinical trials. Future work should prioritize standardized protocols, biomarker-guided personalization, combination strategies (diet/priming), and development of defined microbial therapeutics to improve efficacy and safety.
Additional Links: PMID-41798257
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@article {pmid41798257,
year = {2026},
author = {Liu, J and Wu, X},
title = {Fecal microbiota transplantation in ulcerative colitis: evidence, mechanisms, and practice considerations.},
journal = {Therapeutic advances in gastroenterology},
volume = {19},
number = {},
pages = {17562848261426284},
pmid = {41798257},
issn = {1756-283X},
abstract = {Ulcerative colitis (UC) is a chronic inflammatory bowel disease strongly associated with intestinal dysbiosis, reduced microbial diversity, and disrupted microbial metabolite profiles. Fecal microbiota transplantation (FMT) aims to restore microbial homeostasis and has shown a signal of benefit for induction of remission in some trials, but results are heterogeneous and long-term maintenance efficacy remains uncertain. In this narrative review, we synthesize randomized controlled trials (RCTs), systematic reviews/meta-analyses, and recent guideline and regulatory updates on FMT in UC, and integrate mechanistic insights from microbiome and metabolomics research. Across RCTs, intensive lower-gastrointestinal regimens using pooled, multidonor material, and/or anaerobic processing have most consistently achieved modestly higher steroid-free clinical and endoscopic remission than placebo in mild-to-moderate UC (approximately 25%-32% vs 5%-10% in representative studies), whereas upper-gastrointestinal delivery or oral lyophilized formulations and highly restrictive donor selection have yielded mixed or negative results. Mechanistically, responders commonly demonstrate engraftment of short-chain fatty acid producing taxa and restoration of secondary bile acid pathways. Safety profiles in trials are generally comparable to placebo for common mild adverse events, but rare severe transmissions (e.g., multidrug-resistant Escherichia coli and SARS-CoV-2) have driven stricter donor screening and have limited routine use outside regulated programs. Current guidelines recommend against FMT for UC outside clinical trials. Future work should prioritize standardized protocols, biomarker-guided personalization, combination strategies (diet/priming), and development of defined microbial therapeutics to improve efficacy and safety.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
The impact of gut microbiota on leukemia and prospects for novel therapies.
Infectious medicine, 5(1):100239.
The Human Microbiome Project has underscored the pivotal role of the gut microbiome in human health, revealing its potential influence on leukemia development, progression, and treatment response. This review summarizes evidence on microbiome-targeted therapies such as probiotics, fecal microbiota transplantation, antimicrobial peptides, and nanoparticles. These approaches may improve leukemia treatment outcomes through immune and metabolic modulation and reduced toxicity. Although emerging data suggest beneficial effects, most findings remain correlative and limited by small, heterogeneous studies. Further mechanistic and clinical research is required to clarify causal pathways, standardize interventions, and evaluate long-term safety. Personalized microbiome-based strategies that integrate molecular and immunologic profiling may ultimately refine leukemia management and improve survival.
Additional Links: PMID-41797849
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Citation:
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@article {pmid41797849,
year = {2026},
author = {Jalalifar, S and Bajelan, B and Mohammadi, R and Ghafoury, R and Kalhori, Z and Pooshang-Bagheri, K and Nekouian, R and Faranoush, M},
title = {The impact of gut microbiota on leukemia and prospects for novel therapies.},
journal = {Infectious medicine},
volume = {5},
number = {1},
pages = {100239},
pmid = {41797849},
issn = {2772-431X},
abstract = {The Human Microbiome Project has underscored the pivotal role of the gut microbiome in human health, revealing its potential influence on leukemia development, progression, and treatment response. This review summarizes evidence on microbiome-targeted therapies such as probiotics, fecal microbiota transplantation, antimicrobial peptides, and nanoparticles. These approaches may improve leukemia treatment outcomes through immune and metabolic modulation and reduced toxicity. Although emerging data suggest beneficial effects, most findings remain correlative and limited by small, heterogeneous studies. Further mechanistic and clinical research is required to clarify causal pathways, standardize interventions, and evaluate long-term safety. Personalized microbiome-based strategies that integrate molecular and immunologic profiling may ultimately refine leukemia management and improve survival.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Cold exposure and human metabolism: A heterogeneous response across tissues and organs.
Temperature (Austin, Tex.), 13(1):15-50.
Cold-induced metabolic responses across human organs and tissues vary markedly and do not regulate metabolism uniformly. The magnitude and nature of these responses differ depending on the type of cold exposure, ranging from mild surface cooling and beta-adrenergic stimulation to deep tissue cooling impacting intracellular biophysical and metabolic properties. Upregulating brown adipose tissue (BAT) activity has been proposed to improve whole-body metabolism. Despite its high metabolic activity, BAT mass is typically only 50-100 g and may contribute less than 1% of total heat production during thermogenesis. In contrast, skeletal muscles and white adipocytes may play greater roles in thermogenic and metabolic regulation. Cold exposure triggers a cascade of metabolic responses across tissues, extending beyond fuel partitioning and the regulation of uncoupling proteins. It also alters gene expression, protein synthesis, and metabolic pathways. In response to cold, the body increases sympathetic nervous system activity, leading to peripheral vasoconstriction and energy substrate mobilization. Brown adipocytes increase mitochondrial uncoupling to produce heat, while skeletal muscle contributes through shivering and non-shivering thermogenesis. The liver adjusts glucose production and lipid metabolism, the heart and circulatory system adapt to altered hemodynamic demands, and the kidneys modify fluid balance. Endocrine systems, including the thyroid, amplify thermogenic capacity, and the brain integrates thermal sensing with behavioral responses. Cold exposure also modulates immune function, cytokine profiles and inflammatory pathways across tissues, and shifts in gut microbiome composition influence nutrient absorption, bile acid metabolism and energy homeostasis. These coordinated tissue-specific adaptations enable the maintenance of core temperature during cold stress.
Additional Links: PMID-41797814
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Citation:
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@article {pmid41797814,
year = {2026},
author = {Tetzlaff, EJ and Hancock, C and Waddell, L and Gagnon, SS and Mäkelä, KA and Karhu, T and Peltonen, JE and Herzig, KH and Gagnon, DD},
title = {Cold exposure and human metabolism: A heterogeneous response across tissues and organs.},
journal = {Temperature (Austin, Tex.)},
volume = {13},
number = {1},
pages = {15-50},
pmid = {41797814},
issn = {2332-8940},
abstract = {Cold-induced metabolic responses across human organs and tissues vary markedly and do not regulate metabolism uniformly. The magnitude and nature of these responses differ depending on the type of cold exposure, ranging from mild surface cooling and beta-adrenergic stimulation to deep tissue cooling impacting intracellular biophysical and metabolic properties. Upregulating brown adipose tissue (BAT) activity has been proposed to improve whole-body metabolism. Despite its high metabolic activity, BAT mass is typically only 50-100 g and may contribute less than 1% of total heat production during thermogenesis. In contrast, skeletal muscles and white adipocytes may play greater roles in thermogenic and metabolic regulation. Cold exposure triggers a cascade of metabolic responses across tissues, extending beyond fuel partitioning and the regulation of uncoupling proteins. It also alters gene expression, protein synthesis, and metabolic pathways. In response to cold, the body increases sympathetic nervous system activity, leading to peripheral vasoconstriction and energy substrate mobilization. Brown adipocytes increase mitochondrial uncoupling to produce heat, while skeletal muscle contributes through shivering and non-shivering thermogenesis. The liver adjusts glucose production and lipid metabolism, the heart and circulatory system adapt to altered hemodynamic demands, and the kidneys modify fluid balance. Endocrine systems, including the thyroid, amplify thermogenic capacity, and the brain integrates thermal sensing with behavioral responses. Cold exposure also modulates immune function, cytokine profiles and inflammatory pathways across tissues, and shifts in gut microbiome composition influence nutrient absorption, bile acid metabolism and energy homeostasis. These coordinated tissue-specific adaptations enable the maintenance of core temperature during cold stress.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Gut microbiota and sarcoidosis: a concise review.
Frontiers in medicine, 13:1747012.
Microbial involvement in sarcoidosis pathogenesis is suggested by the observation that histological findings in sarcoid granulomas are like those of leprosy, tuberculosis and parasitic infection. Some studies have shown that the lung microbiome in patients with sarcoidosis is different from healthy individuals. Results are conflicting, reporting an abundance or decrease in bacterial and fungal species. The altered composition of the microbiome in sarcoidosis can contribute to the formation of granulomas, typical lesions of the disease, through interactions with the host immune system. However, no single microbe has been clearly demonstrated as a cause of sarcoidosis, several microorganisms have been involved in the formation of granulomas and are under study. In fact, various microorganisms have been detected in sarcoid granulomas and in the tissue of different organs. Microorganisms were demonstrated at the genomic level and only a few studies showed microbial presence using bacteriological or proteomic methods. A possible microbial involvement in sarcoidosis pathogenesis is further supported by studies reporting innate immune system activation and increased inflammatory cytokines secretion. Of note, a meta-analysis involving over 6,000 patients identified a strong association between Cutibacterium acnes and Mycobacterium tuberculosis and sarcoidosis. Interestingly, some studies have compared microbiomes in sarcoidosis with chronic respiratory conditions like chronic obstructive pulmonary disease, asthma, interstitial lung disease, and occupational lung diseases. Little is known whether gut microbiota alteration plays a causal role in the development of these diseases or is a consequence of a shared risk factor profile. However, current evidence does not conclusively support the causative role of microbes in sarcoidosis. Furthermore, research is studying the role of intestinal microbiomes in sarcoidosis with some studies showing that the restoration of the intestinal microbiome could be a possible therapeutic approach. The aims of the review are: (1) to clarify microbial involvement in sarcoidosis pathogenesis, (2) to describe microbiota in lungs of patients with sarcoidosis and to compare the data with other interstitial lung diseases.
Additional Links: PMID-41797790
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@article {pmid41797790,
year = {2026},
author = {Carbone, RG and Puppo, F and Tapson, VF},
title = {Gut microbiota and sarcoidosis: a concise review.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1747012},
pmid = {41797790},
issn = {2296-858X},
abstract = {Microbial involvement in sarcoidosis pathogenesis is suggested by the observation that histological findings in sarcoid granulomas are like those of leprosy, tuberculosis and parasitic infection. Some studies have shown that the lung microbiome in patients with sarcoidosis is different from healthy individuals. Results are conflicting, reporting an abundance or decrease in bacterial and fungal species. The altered composition of the microbiome in sarcoidosis can contribute to the formation of granulomas, typical lesions of the disease, through interactions with the host immune system. However, no single microbe has been clearly demonstrated as a cause of sarcoidosis, several microorganisms have been involved in the formation of granulomas and are under study. In fact, various microorganisms have been detected in sarcoid granulomas and in the tissue of different organs. Microorganisms were demonstrated at the genomic level and only a few studies showed microbial presence using bacteriological or proteomic methods. A possible microbial involvement in sarcoidosis pathogenesis is further supported by studies reporting innate immune system activation and increased inflammatory cytokines secretion. Of note, a meta-analysis involving over 6,000 patients identified a strong association between Cutibacterium acnes and Mycobacterium tuberculosis and sarcoidosis. Interestingly, some studies have compared microbiomes in sarcoidosis with chronic respiratory conditions like chronic obstructive pulmonary disease, asthma, interstitial lung disease, and occupational lung diseases. Little is known whether gut microbiota alteration plays a causal role in the development of these diseases or is a consequence of a shared risk factor profile. However, current evidence does not conclusively support the causative role of microbes in sarcoidosis. Furthermore, research is studying the role of intestinal microbiomes in sarcoidosis with some studies showing that the restoration of the intestinal microbiome could be a possible therapeutic approach. The aims of the review are: (1) to clarify microbial involvement in sarcoidosis pathogenesis, (2) to describe microbiota in lungs of patients with sarcoidosis and to compare the data with other interstitial lung diseases.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Gut Microbiome Dysbiosis Promotes Gallstone Formation via Bile Acid Metabolic Disorder: A Multiomics Study.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 40(6):e71656.
Gallstone disease is a common global digestive disorder. This study intends to analyze gut microbiota-gallstone disease interactions, to inform disease mechanism and microbiota-targeted prevention and treatment strategies. Participants were recruited from health check-up populations, outpatients, and inpatients. Basic information and biological samples were collected: fecal samples for metagenomic sequencing, and serum samples for bile acid metabolism detection. A total of 62 gallstone patients and 62 healthy controls were enrolled in this study. Compared with the control group, gallstone patients exhibited increased level of bile salt hydrolase (BSH)-producing bacteria, including the genera Bacteroides, Enterococcus, Bifidobacterium, and the family Lactobacillaceae. Further KEGG analysis revealed that the significantly enriched signaling pathways in the gallstone patients were mainly related to bile acid biosynthesis, lipid and bile acid precursor metabolism. Subsequently, we found that in gallstone patients, the levels of hydrophobic bile acids, (e.g., lithocholic acid, LCA), was increased, while the levels of hydrophilic bile acids taurolithocholic acid (TLCA) were decreased. In the correlation analysis between differential bile acids and differential bacterial species, Bacteroides intestinalis was positively correlated with LCA, while Bacteroides fragilis was negatively correlated with TLCA. These results further confirm the role of BSH-active bacteria in bile acid dysregulation. This study proposes the "intestinal microbiota imbalance-bile acid metabolic disorder-gallbladder stone formation" axis, and confirms that gallstone patients exhibit intestinal dysbiosis, which leads to bile acid dysregulation. Furthermore, the accumulation of hydrophobic bile acids is identified as a key factor in gallbladder stone formation.
Additional Links: PMID-41797508
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@article {pmid41797508,
year = {2026},
author = {Huang, C and Xiao, W and Zhao, J and Zhong, R and Gao, L and Ma, H and Tian, L and Yue, P and Lin, Y and He, Q and Xia, B and Yuan, J and Yang, M and Meng, W},
title = {Gut Microbiome Dysbiosis Promotes Gallstone Formation via Bile Acid Metabolic Disorder: A Multiomics Study.},
journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
volume = {40},
number = {6},
pages = {e71656},
pmid = {41797508},
issn = {1530-6860},
support = {82204123//MOST | National Natural Science Foundation of China (NSFC)/ ; 82473707//MOST | National Natural Science Foundation of China (NSFC)/ ; LCYSSQ20220823091203008//Funding of Shenzhen Clinical Research Center for Gastroenterlogy (Gastrointestinal Surgery)/ ; 2022YFC2407405//MOST | National Key Research and Development Program of China (NKPs)/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Bile Acids and Salts/metabolism ; *Dysbiosis/microbiology/metabolism/complications ; *Gallstones/microbiology/metabolism/etiology ; Male ; Female ; Middle Aged ; Feces/microbiology ; Adult ; Aged ; Multiomics ; Amidohydrolases ; },
abstract = {Gallstone disease is a common global digestive disorder. This study intends to analyze gut microbiota-gallstone disease interactions, to inform disease mechanism and microbiota-targeted prevention and treatment strategies. Participants were recruited from health check-up populations, outpatients, and inpatients. Basic information and biological samples were collected: fecal samples for metagenomic sequencing, and serum samples for bile acid metabolism detection. A total of 62 gallstone patients and 62 healthy controls were enrolled in this study. Compared with the control group, gallstone patients exhibited increased level of bile salt hydrolase (BSH)-producing bacteria, including the genera Bacteroides, Enterococcus, Bifidobacterium, and the family Lactobacillaceae. Further KEGG analysis revealed that the significantly enriched signaling pathways in the gallstone patients were mainly related to bile acid biosynthesis, lipid and bile acid precursor metabolism. Subsequently, we found that in gallstone patients, the levels of hydrophobic bile acids, (e.g., lithocholic acid, LCA), was increased, while the levels of hydrophilic bile acids taurolithocholic acid (TLCA) were decreased. In the correlation analysis between differential bile acids and differential bacterial species, Bacteroides intestinalis was positively correlated with LCA, while Bacteroides fragilis was negatively correlated with TLCA. These results further confirm the role of BSH-active bacteria in bile acid dysregulation. This study proposes the "intestinal microbiota imbalance-bile acid metabolic disorder-gallbladder stone formation" axis, and confirms that gallstone patients exhibit intestinal dysbiosis, which leads to bile acid dysregulation. Furthermore, the accumulation of hydrophobic bile acids is identified as a key factor in gallbladder stone formation.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome/physiology
*Bile Acids and Salts/metabolism
*Dysbiosis/microbiology/metabolism/complications
*Gallstones/microbiology/metabolism/etiology
Male
Female
Middle Aged
Feces/microbiology
Adult
Aged
Multiomics
Amidohydrolases
RevDate: 2026-03-09
CmpDate: 2026-03-09
Human Intestinal Microbiota Composition Shapes Model Polyfluoroalkyl Substance Biotransformation.
Chembiochem : a European journal of chemical biology, 27(5):e202500905.
6:2 polyfluoroalkyl phosphate diester (6:2 diPAP) is a prevalent environmental contaminant to which humans are regularly exposed. Environmental microbes can biotransform 6:2 diPAP, and the human gut microbiome can biotransform its congener, 8:2 monoPAP. While the human gut microbiome is highly variable between individuals, potential variability in PAP biotransformation has yet to be assessed. We address this gap using six cohorts (A-F) to examine in vitro biotransformation of 6:2 diPAP by the human gut microbiome. Biotransformation pathways of 6:2 diPAP and their connections to the composition of microbial taxa were assessed using gas chromatography mass spectrometry (GC-MS), liquid chromatography tandem mass spectrometry (LC-MS/MS) and 16S rRNA amplicon sequencing. All cohorts biotransformed 6:2 diPAP but differed in their downstream perfluoroalkyl acid (PFAA) profiles, suggesting diverse biotransformation pathways. Microbial community analysis showed similar alpha diversity across cohorts, while the degree of difference between cohorts varied. The analysis confirmed the initial composition of each cohort's microbial community had a bearing on products stemming from 6:2 diPAP transformation, likely driven by low-abundance microbial taxa. These findings underscore the complexity of microbe-mediated polyfluoroalkyl substance (PFAS) transformation and highlight the need for mechanistic studies that identify the genetic controls governing PFAS transformations in the gut microbiome.
Additional Links: PMID-41797364
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@article {pmid41797364,
year = {2026},
author = {Peskett, ST and Grégoire, DS and Rand, AA},
title = {Human Intestinal Microbiota Composition Shapes Model Polyfluoroalkyl Substance Biotransformation.},
journal = {Chembiochem : a European journal of chemical biology},
volume = {27},
number = {5},
pages = {e202500905},
pmid = {41797364},
issn = {1439-7633},
support = {RGPIN-2018-05330//Natural Science and Engineering Research Council/ ; NFRFE-2023-00695//New Frontiers in Research Fund/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome ; Biotransformation ; RNA, Ribosomal, 16S/genetics ; Tandem Mass Spectrometry ; *Organophosphates/metabolism/chemistry ; *Fluorocarbons/metabolism ; },
abstract = {6:2 polyfluoroalkyl phosphate diester (6:2 diPAP) is a prevalent environmental contaminant to which humans are regularly exposed. Environmental microbes can biotransform 6:2 diPAP, and the human gut microbiome can biotransform its congener, 8:2 monoPAP. While the human gut microbiome is highly variable between individuals, potential variability in PAP biotransformation has yet to be assessed. We address this gap using six cohorts (A-F) to examine in vitro biotransformation of 6:2 diPAP by the human gut microbiome. Biotransformation pathways of 6:2 diPAP and their connections to the composition of microbial taxa were assessed using gas chromatography mass spectrometry (GC-MS), liquid chromatography tandem mass spectrometry (LC-MS/MS) and 16S rRNA amplicon sequencing. All cohorts biotransformed 6:2 diPAP but differed in their downstream perfluoroalkyl acid (PFAA) profiles, suggesting diverse biotransformation pathways. Microbial community analysis showed similar alpha diversity across cohorts, while the degree of difference between cohorts varied. The analysis confirmed the initial composition of each cohort's microbial community had a bearing on products stemming from 6:2 diPAP transformation, likely driven by low-abundance microbial taxa. These findings underscore the complexity of microbe-mediated polyfluoroalkyl substance (PFAS) transformation and highlight the need for mechanistic studies that identify the genetic controls governing PFAS transformations in the gut microbiome.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome
Biotransformation
RNA, Ribosomal, 16S/genetics
Tandem Mass Spectrometry
*Organophosphates/metabolism/chemistry
*Fluorocarbons/metabolism
RevDate: 2026-03-09
Infertility and Periodontitis: Are We Connecting the Right Dots?.
Journal of dental research [Epub ahead of print].
Infertility is an increasing global health concern. Growing evidence suggests that systemic inflammatory conditions, including periodontal disease, may contribute to impaired reproductive outcomes. This narrative review highlights recent conceptual advances linking periodontal disease with male and female infertility, focusing on biological mechanisms (i.e., microbial translocation, chronic inflammation, immune dysregulation, oxidative stress, and epigenetic modifications). The review critically examines available studies focusing on scientific quality, design, and clinical relevance. In females, periodontal disease has been associated with idiopathic infertility and polycystic ovary syndrome. These conditions are characterized by immune dysregulation and low-grade systemic inflammation. In males, impaired semen parameters and idiopathic infertility have been linked to poor periodontal status. Despite growing interest, existing studies are largely associative and limited by methodological heterogeneity, insufficient control for confounders, and a lack of standardized outcome measures. This review proposes a framework for improved future research strategies addressing these shortcomings to clarify causality and therapeutic potential.
Additional Links: PMID-41797218
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PubMed:
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@article {pmid41797218,
year = {2026},
author = {Wetzel, C and Bumm, CV and Becker, J and Schwendicke, F and Folwaczny, M and Werner, N},
title = {Infertility and Periodontitis: Are We Connecting the Right Dots?.},
journal = {Journal of dental research},
volume = {},
number = {},
pages = {220345261416502},
doi = {10.1177/00220345261416502},
pmid = {41797218},
issn = {1544-0591},
abstract = {Infertility is an increasing global health concern. Growing evidence suggests that systemic inflammatory conditions, including periodontal disease, may contribute to impaired reproductive outcomes. This narrative review highlights recent conceptual advances linking periodontal disease with male and female infertility, focusing on biological mechanisms (i.e., microbial translocation, chronic inflammation, immune dysregulation, oxidative stress, and epigenetic modifications). The review critically examines available studies focusing on scientific quality, design, and clinical relevance. In females, periodontal disease has been associated with idiopathic infertility and polycystic ovary syndrome. These conditions are characterized by immune dysregulation and low-grade systemic inflammation. In males, impaired semen parameters and idiopathic infertility have been linked to poor periodontal status. Despite growing interest, existing studies are largely associative and limited by methodological heterogeneity, insufficient control for confounders, and a lack of standardized outcome measures. This review proposes a framework for improved future research strategies addressing these shortcomings to clarify causality and therapeutic potential.},
}
RevDate: 2026-03-09
Silkworm excrement-immobilized bacteria for synergistic remediation of phthalate esters in agricultural soil.
Journal of hazardous materials, 507:141703 pii:S0304-3894(26)00681-3 [Epub ahead of print].
The widespread contamination of agricultural soils by phthalate esters (PAEs) poses serious risks to ecosystem and human health. While microbial remediation is a promising solution, the poor survival and performance of free degrading bacteria in complex soil environments limit its practical application. To address this challenge, we develop a novel immobilized inoculant by leveraging silkworm excrement (SE), an agricultural by-product, as a carrier for the efficient PAE-degrader Pseudomonas aeruginosa PS1. This microbe-immobilized silkworm excrement (MSE) was thoroughly characterized and validated by pot experiments. The results showed that MSE treatment significantly reduced PAEs in both soil and choysum (Brassica parachinensis L.), with PAEs detected little in shoots (edible parts), significantly outperforming the treatments of free bacteria or SE alone. The enhanced remediation was linked to MSE-induced improvements in soil health, including increased pH, organic matter, and ammonium nitrogen. Crucially, high-throughput sequencing revealed that MSE application selectively enriched key PAE-degrading bacterial phyla, particularly Proteobacteria and Bacteroidetes, thereby reshaping the soil microbiome into a more effective remediation consortium. This study presents a sustainable and efficient bioaugmentation strategy for transforming a waste product into a functional inoculant, offering a viable solution for the in-situ remediation of PAE-contaminated soils.
Additional Links: PMID-41797118
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PubMed:
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@article {pmid41797118,
year = {2026},
author = {Chen, YH and Du, H and Liu, YX and Xu, K and Ye, JC and Liu, BL and Feng, NX and Xiang, L and Li, YW and Cai, QY and Mo, CH and Zhao, HM},
title = {Silkworm excrement-immobilized bacteria for synergistic remediation of phthalate esters in agricultural soil.},
journal = {Journal of hazardous materials},
volume = {507},
number = {},
pages = {141703},
doi = {10.1016/j.jhazmat.2026.141703},
pmid = {41797118},
issn = {1873-3336},
abstract = {The widespread contamination of agricultural soils by phthalate esters (PAEs) poses serious risks to ecosystem and human health. While microbial remediation is a promising solution, the poor survival and performance of free degrading bacteria in complex soil environments limit its practical application. To address this challenge, we develop a novel immobilized inoculant by leveraging silkworm excrement (SE), an agricultural by-product, as a carrier for the efficient PAE-degrader Pseudomonas aeruginosa PS1. This microbe-immobilized silkworm excrement (MSE) was thoroughly characterized and validated by pot experiments. The results showed that MSE treatment significantly reduced PAEs in both soil and choysum (Brassica parachinensis L.), with PAEs detected little in shoots (edible parts), significantly outperforming the treatments of free bacteria or SE alone. The enhanced remediation was linked to MSE-induced improvements in soil health, including increased pH, organic matter, and ammonium nitrogen. Crucially, high-throughput sequencing revealed that MSE application selectively enriched key PAE-degrading bacterial phyla, particularly Proteobacteria and Bacteroidetes, thereby reshaping the soil microbiome into a more effective remediation consortium. This study presents a sustainable and efficient bioaugmentation strategy for transforming a waste product into a functional inoculant, offering a viable solution for the in-situ remediation of PAE-contaminated soils.},
}
RevDate: 2026-03-09
Role of the gut microbiome in shaping drug response in immunocompromised hosts.
Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases pii:S1198-743X(26)00104-7 [Epub ahead of print].
BACKGROUND: There is an increasing amount of evidence on microbiome-drug interactions in several clinical settings, including in immunocompromised patients. The gut microbiome has been shown to directly and indirectly influence drug efficacy and toxicity, offering high potential for clinical translation.
OBJECTIVES: This narrative review aims to provide an up-to-date overview of the relationship between gut microbes and drugs, with a focus on immu1no-chemotherapy in immunocompromised hosts, including oncological and transplant patients.
SOURCES: We searched PubMed to identify relevant literature in English up to February 2026, as well as included articles known to the authors (prioritising clinical studies wherever possible).
CONTENT: For commonly used anticancer drugs in untargeted conventional chemotherapy, gut microbes may directly activate prodrugs, inactivate biologically active drugs, and/or interfere with their toxicity. Furthermore, indirect mechanisms of immune system modulation have been shown to enhance or worsen therapeutic outcomes, including in targeted immunotherapy. For immunosuppressants in transplant recipients, there is less available evidence overall. Nevertheless, existing studies support the role of the gut microbiome in influencing pharmacokinetics, including enterohepatic recirculation, also through modulation of host drug-metabolising enzymes. Notably, some studies have demonstrated the potential of targeted microbiome manipulation to improve therapeutic outcomes. However, most of this information derives from small, heterogeneous studies, including animal models and in vitro studies.
IMPLICATIONS: The translational implications of microbiome research in pharmacology are of paramount importance. Well-designed clinical studies and the integration of in vivo and ex vivo models will be essential for advancing knowledge and providing mechanistic insights into microbiome-drug interactions. In parallel, advanced computational approaches such as artificial intelligence and machine learning tools will facilitate the analysis of complex microbiome data. These approaches will help identify clinically relevant microbial signatures, including high-risk microbiome-drug interactions. This will enable the development of personalised precision strategies to improve clinical outcomes and prolong disease-free survival.
Additional Links: PMID-41796961
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PubMed:
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@article {pmid41796961,
year = {2026},
author = {Bejaoui, S and D'Amico, F and Turroni, S},
title = {Role of the gut microbiome in shaping drug response in immunocompromised hosts.},
journal = {Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cmi.2026.02.026},
pmid = {41796961},
issn = {1469-0691},
abstract = {BACKGROUND: There is an increasing amount of evidence on microbiome-drug interactions in several clinical settings, including in immunocompromised patients. The gut microbiome has been shown to directly and indirectly influence drug efficacy and toxicity, offering high potential for clinical translation.
OBJECTIVES: This narrative review aims to provide an up-to-date overview of the relationship between gut microbes and drugs, with a focus on immu1no-chemotherapy in immunocompromised hosts, including oncological and transplant patients.
SOURCES: We searched PubMed to identify relevant literature in English up to February 2026, as well as included articles known to the authors (prioritising clinical studies wherever possible).
CONTENT: For commonly used anticancer drugs in untargeted conventional chemotherapy, gut microbes may directly activate prodrugs, inactivate biologically active drugs, and/or interfere with their toxicity. Furthermore, indirect mechanisms of immune system modulation have been shown to enhance or worsen therapeutic outcomes, including in targeted immunotherapy. For immunosuppressants in transplant recipients, there is less available evidence overall. Nevertheless, existing studies support the role of the gut microbiome in influencing pharmacokinetics, including enterohepatic recirculation, also through modulation of host drug-metabolising enzymes. Notably, some studies have demonstrated the potential of targeted microbiome manipulation to improve therapeutic outcomes. However, most of this information derives from small, heterogeneous studies, including animal models and in vitro studies.
IMPLICATIONS: The translational implications of microbiome research in pharmacology are of paramount importance. Well-designed clinical studies and the integration of in vivo and ex vivo models will be essential for advancing knowledge and providing mechanistic insights into microbiome-drug interactions. In parallel, advanced computational approaches such as artificial intelligence and machine learning tools will facilitate the analysis of complex microbiome data. These approaches will help identify clinically relevant microbial signatures, including high-risk microbiome-drug interactions. This will enable the development of personalised precision strategies to improve clinical outcomes and prolong disease-free survival.},
}
RevDate: 2026-03-09
Effects of Fluoride Chemical Forms of Sodium Fluoride and Monofluorophosphate on Microbial Viability and Diversity in Saliva-Derived Biofilms.
Journal of dentistry pii:S0300-5712(26)00287-3 [Epub ahead of print].
OBJECTIVES: Fluorides are widely used for caries prevention; however, knowledge of the differences in their chemical speciation and associated microbiological effects remains incomplete. This study aimed to elucidate the ionization behavior of sodium fluoride (NaF) and sodium monofluorophosphate (MFP) using [19]F NMR spectroscopy and to evaluate their effects on biofilm growth, viability, and microbial composition in saliva-derived polymicrobial biofilms.
METHODS: The chemical speciation of NaF and MFP solutions was characterized by [19]F NMR spectroscopy. Polymicrobial biofilms were established from human saliva using an in vitro biofilm model on hydroxyapatite discs. Biofilms were then exposed to NaF or MFP at an equivalent fluoride concentration (1450 ppm). Microbial viability was assessed using an ATP-based luminescence assay. Biofilm community composition was analyzed by 16S rRNA gene sequencing, followed by diversity and differential abundance analyses.
RESULTS: [19]F NMR analysis demonstrated that NaF fully dissociated into free fluoride ions, whereas MFP existed predominantly as monofluorophosphate ions, with only a small fraction of free fluoride. Both fluoride compounds significantly reduced microbial viability. NaF exerted a strong, non-selective inhibitory effect without significantly altering overall community structure or alpha diversity. In contrast, MFP caused selective suppression of specific taxa and significantly decreased Shannon diversity. Differential abundance analysis confirmed compound-specific shifts in bacterial genera, indicating distinct antimicrobial profiles.
CONCLUSIONS: NaF and MFP exhibited differential antibiofilm effects, with NaF causing a greater reduction in microbial viability than MFP. 16S rRNA analysis revealed that NaF had minimal impact on the overall microbial composition, whereas MFP induced selective changes in bacterial taxa.
CLINICAL SIGNIFICANCE: This study revealed that fluoride compounds exhibit different antibiofilm effects due to their distinct chemical forms. These forms were precisely identified using [19]F NMR rather than conventional fluoride ion-selective electrodes. These findings may help improve understanding of fluoride behavior and guide future research in caries prevention.
Additional Links: PMID-41796931
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PubMed:
Citation:
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@article {pmid41796931,
year = {2026},
author = {Gondo, T and Abe, S and Hiraishi, N and Hayashi, F and Okazaki, Y and Abe, T and Shimabukuro, M and Moyes, D and Hill, RG and Shimada, Y},
title = {Effects of Fluoride Chemical Forms of Sodium Fluoride and Monofluorophosphate on Microbial Viability and Diversity in Saliva-Derived Biofilms.},
journal = {Journal of dentistry},
volume = {},
number = {},
pages = {106615},
doi = {10.1016/j.jdent.2026.106615},
pmid = {41796931},
issn = {1879-176X},
abstract = {OBJECTIVES: Fluorides are widely used for caries prevention; however, knowledge of the differences in their chemical speciation and associated microbiological effects remains incomplete. This study aimed to elucidate the ionization behavior of sodium fluoride (NaF) and sodium monofluorophosphate (MFP) using [19]F NMR spectroscopy and to evaluate their effects on biofilm growth, viability, and microbial composition in saliva-derived polymicrobial biofilms.
METHODS: The chemical speciation of NaF and MFP solutions was characterized by [19]F NMR spectroscopy. Polymicrobial biofilms were established from human saliva using an in vitro biofilm model on hydroxyapatite discs. Biofilms were then exposed to NaF or MFP at an equivalent fluoride concentration (1450 ppm). Microbial viability was assessed using an ATP-based luminescence assay. Biofilm community composition was analyzed by 16S rRNA gene sequencing, followed by diversity and differential abundance analyses.
RESULTS: [19]F NMR analysis demonstrated that NaF fully dissociated into free fluoride ions, whereas MFP existed predominantly as monofluorophosphate ions, with only a small fraction of free fluoride. Both fluoride compounds significantly reduced microbial viability. NaF exerted a strong, non-selective inhibitory effect without significantly altering overall community structure or alpha diversity. In contrast, MFP caused selective suppression of specific taxa and significantly decreased Shannon diversity. Differential abundance analysis confirmed compound-specific shifts in bacterial genera, indicating distinct antimicrobial profiles.
CONCLUSIONS: NaF and MFP exhibited differential antibiofilm effects, with NaF causing a greater reduction in microbial viability than MFP. 16S rRNA analysis revealed that NaF had minimal impact on the overall microbial composition, whereas MFP induced selective changes in bacterial taxa.
CLINICAL SIGNIFICANCE: This study revealed that fluoride compounds exhibit different antibiofilm effects due to their distinct chemical forms. These forms were precisely identified using [19]F NMR rather than conventional fluoride ion-selective electrodes. These findings may help improve understanding of fluoride behavior and guide future research in caries prevention.},
}
RevDate: 2026-03-09
Vagus nerve stimulation in autoimmune diseases: Mechanisms, therapeutic potential, and clinical applications.
Autoimmunity reviews pii:S1568-9972(26)00037-6 [Epub ahead of print].
Autoimmune diseases characterized by dysregulated immune responses against self-antigens. Current pharmacotherapies are limited by like resistance, side effects, and high costs, highlighting the need for novel interventions. Vagus nerve stimulation (VNS) offers a promising alternative through three forms, including implantable, transcutaneous cervical, and transcutaneous auricular. Increasing clinical evidence demonstrates VNS benefits patients with autoimmune disorders, such as treatment-refractory rheumatoid arthritis, Crohn's disease, and systemic lupus erythematosus. Preclinical studies support that VNS attenuates inflammation primarily via the cholinergic anti-inflammatory pathway (CAP) through α7 nicotinic acetylcholine receptor (α7nAChR) activation. Emerging insights implicate β-adrenergic signaling, hypothalamic-pituitary-adrenal (HPA) axis modulation, and gut microbiome regulation. This review summarizes current clinical and preclinical evidence, synthesizes current mechanistic understanding, and addresses key gaps in clinical validation. Future research priorities include conducting large-scale randomized controlled trials to extend VNS applications to broader autoimmune diseases and advancing the neurostimulation efficacy of non-invasive vagus nerve stimulation devices.
Additional Links: PMID-41796720
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PubMed:
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@article {pmid41796720,
year = {2026},
author = {Ye, J and Lan, Y and Li, W and Lv, H and Wen, C and Xu, Z},
title = {Vagus nerve stimulation in autoimmune diseases: Mechanisms, therapeutic potential, and clinical applications.},
journal = {Autoimmunity reviews},
volume = {},
number = {},
pages = {104023},
doi = {10.1016/j.autrev.2026.104023},
pmid = {41796720},
issn = {1873-0183},
abstract = {Autoimmune diseases characterized by dysregulated immune responses against self-antigens. Current pharmacotherapies are limited by like resistance, side effects, and high costs, highlighting the need for novel interventions. Vagus nerve stimulation (VNS) offers a promising alternative through three forms, including implantable, transcutaneous cervical, and transcutaneous auricular. Increasing clinical evidence demonstrates VNS benefits patients with autoimmune disorders, such as treatment-refractory rheumatoid arthritis, Crohn's disease, and systemic lupus erythematosus. Preclinical studies support that VNS attenuates inflammation primarily via the cholinergic anti-inflammatory pathway (CAP) through α7 nicotinic acetylcholine receptor (α7nAChR) activation. Emerging insights implicate β-adrenergic signaling, hypothalamic-pituitary-adrenal (HPA) axis modulation, and gut microbiome regulation. This review summarizes current clinical and preclinical evidence, synthesizes current mechanistic understanding, and addresses key gaps in clinical validation. Future research priorities include conducting large-scale randomized controlled trials to extend VNS applications to broader autoimmune diseases and advancing the neurostimulation efficacy of non-invasive vagus nerve stimulation devices.},
}
RevDate: 2026-03-10
Functional and metabolic dysbiosis of the gut microbiome in the tumoral immune microenvironment of hepatocellular carcinoma.
Cellular signalling, 143:112455 pii:S0898-6568(26)00105-1 [Epub ahead of print].
With its asymptomatic and heterogeneous nature, hepatocellular carcinoma (HCC) ranks as one of the most fatal malignancies globally, contributing to a deteriorating five-year overall survival. The gut microbiome, as the resident microorganism of the digestive tract, has been linked to a variety of hepatic disorders based on the internal "gut-liver" axis, accompanied by alterations in microbial components and derived metabolites. We found that patients with HCC had a greater abundance of Streptococcus salivarius (S. salivarius) and lithocholic acid (LCA), but its role in the tumor immune microenvironment remains elusive. Methodologically, we conducted 16S rRNA, 5R 16S rRNA sequencing and metabolomic analysis to discern the impact of S. salivarius in C-Myc/NRas-driven HCC mouse model and RNA-sequencing (RNA-seq) was performed to clarify the particular pathophysiological mechanism. In addition, the effect of S. salivarius on the efficacy of Anti-PD1 immunotherapy was evaluated as well. Mechanistically, S. salivarius was demonstrated to impede the cGAS/STING axis, consequently dampening the anti-tumor immune response by restricting the CD8[+] T cell trafficking to tumor microenvironment (TME) and triggering the immunosuppressive factor PD-1. Meanwhile, the integrative analysis indicated that the generated LCA facilitated the translocation of S. salivarius towards tumor site and activated the tumor-associated macrophages (TAMs), which altogether reshaped the immune TME in HCC. Our findings revealed perturbed microbial and metabolic features in the pathogenesis of HCC and offered a motivation for considering potential interventions during patient treatment.
Additional Links: PMID-41796648
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PubMed:
Citation:
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@article {pmid41796648,
year = {2026},
author = {He, Q and Wu, H and Guo, M and Ye, R and Li, H and Zhang, Q},
title = {Functional and metabolic dysbiosis of the gut microbiome in the tumoral immune microenvironment of hepatocellular carcinoma.},
journal = {Cellular signalling},
volume = {143},
number = {},
pages = {112455},
doi = {10.1016/j.cellsig.2026.112455},
pmid = {41796648},
issn = {1873-3913},
abstract = {With its asymptomatic and heterogeneous nature, hepatocellular carcinoma (HCC) ranks as one of the most fatal malignancies globally, contributing to a deteriorating five-year overall survival. The gut microbiome, as the resident microorganism of the digestive tract, has been linked to a variety of hepatic disorders based on the internal "gut-liver" axis, accompanied by alterations in microbial components and derived metabolites. We found that patients with HCC had a greater abundance of Streptococcus salivarius (S. salivarius) and lithocholic acid (LCA), but its role in the tumor immune microenvironment remains elusive. Methodologically, we conducted 16S rRNA, 5R 16S rRNA sequencing and metabolomic analysis to discern the impact of S. salivarius in C-Myc/NRas-driven HCC mouse model and RNA-sequencing (RNA-seq) was performed to clarify the particular pathophysiological mechanism. In addition, the effect of S. salivarius on the efficacy of Anti-PD1 immunotherapy was evaluated as well. Mechanistically, S. salivarius was demonstrated to impede the cGAS/STING axis, consequently dampening the anti-tumor immune response by restricting the CD8[+] T cell trafficking to tumor microenvironment (TME) and triggering the immunosuppressive factor PD-1. Meanwhile, the integrative analysis indicated that the generated LCA facilitated the translocation of S. salivarius towards tumor site and activated the tumor-associated macrophages (TAMs), which altogether reshaped the immune TME in HCC. Our findings revealed perturbed microbial and metabolic features in the pathogenesis of HCC and offered a motivation for considering potential interventions during patient treatment.},
}
RevDate: 2026-03-09
Exploring the gut micriobiome in Anopheles mosquitoes: A promising new approach to malaria control.
Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases pii:S1567-1348(26)00041-9 [Epub ahead of print].
Malaria continues to pose significant public health issues globally. This disease is primarily spread through the bites of female Anopheles mosquitoes that are infected with the Plasmodium parasites. While conventional vector control strategies such as insecticide-treated bed nets (ITNs) and indoor residual spraying (IRS) have significantly reduced malaria burden, their long-term effectiveness is increasingly compromised by widespread insecticide resistance. Recent research has proposed manipulation of the Anopheles gut microbiome as a complementary malaria control strategy; however, the strength, consistency, and translational relevance of this evidence remain uneven. This review goes beyond descriptive synthesis by critically evaluating experimental approaches, identifying methodological limitations, highlighting contradictory findings, and assessing the robustness of current knowledge on mosquito microbiome Plasmodium interactions. We examine bacterial, fungal, and viral components of the Anopheles gut microbiome, emphasizing mechanisms such as immune modulation, nutrient competition, direct antiparasitic activity, and interference with mosquito physiology to inhibit pathogen transmission. Importantly, we identify key caveats, including laboratory bias, oversimplification of microbial consortia, context-dependent outcomes, and ecological uncertainties that challenge the deployment of microbiome-based interventions in the field. By integrating strengths and weaknesses of existing studies, this review provides a balanced and critical framework for future research and responsible translation of microbiome-based malaria control strategies.
Additional Links: PMID-41796626
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PubMed:
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@article {pmid41796626,
year = {2026},
author = {Minwuyelet, A and Atenafu, G},
title = {Exploring the gut micriobiome in Anopheles mosquitoes: A promising new approach to malaria control.},
journal = {Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases},
volume = {},
number = {},
pages = {105917},
doi = {10.1016/j.meegid.2026.105917},
pmid = {41796626},
issn = {1567-7257},
abstract = {Malaria continues to pose significant public health issues globally. This disease is primarily spread through the bites of female Anopheles mosquitoes that are infected with the Plasmodium parasites. While conventional vector control strategies such as insecticide-treated bed nets (ITNs) and indoor residual spraying (IRS) have significantly reduced malaria burden, their long-term effectiveness is increasingly compromised by widespread insecticide resistance. Recent research has proposed manipulation of the Anopheles gut microbiome as a complementary malaria control strategy; however, the strength, consistency, and translational relevance of this evidence remain uneven. This review goes beyond descriptive synthesis by critically evaluating experimental approaches, identifying methodological limitations, highlighting contradictory findings, and assessing the robustness of current knowledge on mosquito microbiome Plasmodium interactions. We examine bacterial, fungal, and viral components of the Anopheles gut microbiome, emphasizing mechanisms such as immune modulation, nutrient competition, direct antiparasitic activity, and interference with mosquito physiology to inhibit pathogen transmission. Importantly, we identify key caveats, including laboratory bias, oversimplification of microbial consortia, context-dependent outcomes, and ecological uncertainties that challenge the deployment of microbiome-based interventions in the field. By integrating strengths and weaknesses of existing studies, this review provides a balanced and critical framework for future research and responsible translation of microbiome-based malaria control strategies.},
}
RevDate: 2026-03-09
An adaptive weight self-distillation deep learning framework for phenotype prediction from longitudinal gut microbiome data.
BMC microbiology pii:10.1186/s12866-026-04922-y [Epub ahead of print].
Additional Links: PMID-41796297
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@article {pmid41796297,
year = {2026},
author = {Shi, K and He, Q and Wang, S and Guo, J},
title = {An adaptive weight self-distillation deep learning framework for phenotype prediction from longitudinal gut microbiome data.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-04922-y},
pmid = {41796297},
issn = {1471-2180},
support = {62562022//National Natural Science Foundation of China/ ; Guike ZY22096025//Special Funds for Guiding Local Scientific and Technological Development by the Central Government/ ; 2025JJA170175//Guangxi Natural Science Foundation/ ; Z-C20241570//Guangxi Health Commission Self-Funded Research Project/ ; },
}
RevDate: 2026-03-09
Microbiome signatures of mangroves and salt marsh halophyte rhizosphere soil sediments: a metagenomic approach.
Scientific reports pii:10.1038/s41598-026-42270-z [Epub ahead of print].
Additional Links: PMID-41796197
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PubMed:
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@article {pmid41796197,
year = {2026},
author = {Sujeeth, NK and Dharani Bommi, KB and Manojkumar, S and Angayarkanni, J and Gnanadesigan, M},
title = {Microbiome signatures of mangroves and salt marsh halophyte rhizosphere soil sediments: a metagenomic approach.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-42270-z},
pmid = {41796197},
issn = {2045-2322},
}
RevDate: 2026-03-08
CmpDate: 2026-03-08
Effects of Lactic Acid Bacteria on Fermentation Quality and Microbiome of Leymus chinensis Silage.
MicrobiologyOpen, 15(2):e70262.
This study investigated the distinct effects of Lentilactobacillus buchneri (LB) and Lactiplantibacillus plantarum (LP) inoculants on the fermentation characteristics and bacterial community succession of Leymus chinensis silage. Treatments included distilled water (CON), LB, and LP, applied at a concentration of 1 × 10[6] cfu/g of fresh matter (FM). Compared with the CON group, the fermentation quality was improved by the inoculations, the markedly (p < 0.05) lower pH and NH3-N were found in the LB and LP treatments. The significantly (p < 0.05) highest LA and AA contents were detected in the LP and LB treatments, respectively. The bacterial diversity, reflected by Shannon and Chao1 indices, decreased throughout the ensiling process, with the LP group exhibiting the most pronounced reduction. Furthermore, beta-diversity analysis revealed distinct microbial community structures among the treatments. While fresh L. chinensis was dominated by Proteobacteria (48.03%), Firmicutes (26.23%), and Actinobacteriota (23.72%), the microbiome shifted dramatically after 60 days of ensiling to be predominantly Firmicutes (94.96%-99.79%), the genus Rhodococcus, Microbacterium, Enterococcus and Leuconostoc, Weissella, and Enterococcus were markedly (p < 0.05) enriched in the CK treatment during fermentation from 3 to 14 days, while from 30 days, the genus Lactobacillus as the dominant genus, especially in the LB and LP treatments. In conclusion, both additives facilitate L. chinensis ensiling by regulating the microbiome, yet L. plantarum demonstrates superior efficacy in optimizing fermentation quality.
Additional Links: PMID-41796087
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@article {pmid41796087,
year = {2026},
author = {Jiang, X and He, L and Han, Z and Zong, S and Du, S and Wu, H and Xiao, Y},
title = {Effects of Lactic Acid Bacteria on Fermentation Quality and Microbiome of Leymus chinensis Silage.},
journal = {MicrobiologyOpen},
volume = {15},
number = {2},
pages = {e70262},
pmid = {41796087},
issn = {2045-8827},
support = {202LHMS03022//Natural Science Foundation of Inner Mongolia/ ; BFGJ2024006//Northern Agriculture and Livestock Husbandry Technical Innovation Center/ ; },
mesh = {*Silage/microbiology/analysis ; *Fermentation ; *Microbiota ; *Poaceae/microbiology/metabolism ; *Lactobacillales/metabolism ; Lactiplantibacillus plantarum/metabolism ; Hydrogen-Ion Concentration ; Bacteria/classification/genetics ; Lactobacillus ; },
abstract = {This study investigated the distinct effects of Lentilactobacillus buchneri (LB) and Lactiplantibacillus plantarum (LP) inoculants on the fermentation characteristics and bacterial community succession of Leymus chinensis silage. Treatments included distilled water (CON), LB, and LP, applied at a concentration of 1 × 10[6] cfu/g of fresh matter (FM). Compared with the CON group, the fermentation quality was improved by the inoculations, the markedly (p < 0.05) lower pH and NH3-N were found in the LB and LP treatments. The significantly (p < 0.05) highest LA and AA contents were detected in the LP and LB treatments, respectively. The bacterial diversity, reflected by Shannon and Chao1 indices, decreased throughout the ensiling process, with the LP group exhibiting the most pronounced reduction. Furthermore, beta-diversity analysis revealed distinct microbial community structures among the treatments. While fresh L. chinensis was dominated by Proteobacteria (48.03%), Firmicutes (26.23%), and Actinobacteriota (23.72%), the microbiome shifted dramatically after 60 days of ensiling to be predominantly Firmicutes (94.96%-99.79%), the genus Rhodococcus, Microbacterium, Enterococcus and Leuconostoc, Weissella, and Enterococcus were markedly (p < 0.05) enriched in the CK treatment during fermentation from 3 to 14 days, while from 30 days, the genus Lactobacillus as the dominant genus, especially in the LB and LP treatments. In conclusion, both additives facilitate L. chinensis ensiling by regulating the microbiome, yet L. plantarum demonstrates superior efficacy in optimizing fermentation quality.},
}
MeSH Terms:
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*Silage/microbiology/analysis
*Fermentation
*Microbiota
*Poaceae/microbiology/metabolism
*Lactobacillales/metabolism
Lactiplantibacillus plantarum/metabolism
Hydrogen-Ion Concentration
Bacteria/classification/genetics
Lactobacillus
RevDate: 2026-03-10
CmpDate: 2026-03-08
The Emerging Role of Gut Microbiota in Inflammatory Skin Diseases: A Systematic Review.
Experimental dermatology, 35(3):e70234.
The human gut microbiota is involved in immune regulation, metabolism, and skin homeostasis. In recent years, gut microbiota alterations have been linked with several inflammatory skin disorders, such as atopic dermatitis (AD), psoriasis, and hidradenitis suppurativa (HS). This systematic review synthesises current evidence on gut microbiota composition and functional alterations in these dermatoses. A comprehensive literature search was conducted in the PubMed database, identifying studies from inception to January 2025. Eligible studies included human observational, interventional, and genetic studies investigating gut microbiota alterations in AD, psoriasis, or HS, using microbiome profiling or genetic causal-inference approaches. Studies lacking control groups or relying on culture-based techniques were excluded. Sixty-two studies were included: 38 on AD, 22 on psoriasis and 5 on HS, with three addressing more than one disease. In AD, most studies focused on paediatric populations, leaving a knowledge gap regarding adult-specific data. Reduced alpha-diversity and decreased abundance of Faecalibacterium prausnitzii, Bifidobacterium spp., and Akkermansia muciniphila were recurrent findings. In psoriasis, in addition to dysbiosis, microbial metabolic pathways were also found to be altered. In HS, data remain limited, but increased Ruminococcus gnavus and reduced alpha-diversity have been reported, mirroring findings in inflammatory bowel diseases. Gut microbiota has been increasingly implicated in skin inflammation. Despite advances in microbiota analysis, significant gaps remain-especially in adult AD and HS. Future research should prioritize standardised methodologies, larger and more diverse cohorts, and leverage emerging tools such as Mendelian randomization and AI-based models to develop precision medicine interventions.
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@article {pmid41795861,
year = {2026},
author = {Malgesini, A and Marsiglia, MD and Borghi, E and Marzano, AV and Nazzaro, G},
title = {The Emerging Role of Gut Microbiota in Inflammatory Skin Diseases: A Systematic Review.},
journal = {Experimental dermatology},
volume = {35},
number = {3},
pages = {e70234},
pmid = {41795861},
issn = {1600-0625},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Psoriasis/microbiology/immunology ; *Hidradenitis Suppurativa/microbiology/immunology ; *Dermatitis, Atopic/microbiology/immunology ; Dysbiosis/microbiology ; },
abstract = {The human gut microbiota is involved in immune regulation, metabolism, and skin homeostasis. In recent years, gut microbiota alterations have been linked with several inflammatory skin disorders, such as atopic dermatitis (AD), psoriasis, and hidradenitis suppurativa (HS). This systematic review synthesises current evidence on gut microbiota composition and functional alterations in these dermatoses. A comprehensive literature search was conducted in the PubMed database, identifying studies from inception to January 2025. Eligible studies included human observational, interventional, and genetic studies investigating gut microbiota alterations in AD, psoriasis, or HS, using microbiome profiling or genetic causal-inference approaches. Studies lacking control groups or relying on culture-based techniques were excluded. Sixty-two studies were included: 38 on AD, 22 on psoriasis and 5 on HS, with three addressing more than one disease. In AD, most studies focused on paediatric populations, leaving a knowledge gap regarding adult-specific data. Reduced alpha-diversity and decreased abundance of Faecalibacterium prausnitzii, Bifidobacterium spp., and Akkermansia muciniphila were recurrent findings. In psoriasis, in addition to dysbiosis, microbial metabolic pathways were also found to be altered. In HS, data remain limited, but increased Ruminococcus gnavus and reduced alpha-diversity have been reported, mirroring findings in inflammatory bowel diseases. Gut microbiota has been increasingly implicated in skin inflammation. Despite advances in microbiota analysis, significant gaps remain-especially in adult AD and HS. Future research should prioritize standardised methodologies, larger and more diverse cohorts, and leverage emerging tools such as Mendelian randomization and AI-based models to develop precision medicine interventions.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome
*Psoriasis/microbiology/immunology
*Hidradenitis Suppurativa/microbiology/immunology
*Dermatitis, Atopic/microbiology/immunology
Dysbiosis/microbiology
RevDate: 2026-03-08
Integration of human microbiota (SIHUMIx) and zebrafish models reveals microbiome-mediated host responses to azoxystrobin.
Toxicological sciences : an official journal of the Society of Toxicology pii:8510753 [Epub ahead of print].
The gut microbiome is essential for neurodevelopment via bidirectional gut-brain axis signaling, yet environmental chemicals can potentially disrupt this communication by altering community structure and xenobiotic metabolism. In this study, we investigated whether the fungicide azoxystrobin, a known metabolic disruptor, modulates microbiome composition and function to influence neurobehavior. We utilized a simplified human gut microbiota model (SIHUMIx) and a vertebrate host model (larval zebrafish) to elucidate microbiome-mediated mechanisms of xenobiotic neurotoxicity. SIHUMIx was exposed to azoxystrobin for 7 days at 10% of the acceptable daily intake, followed by recovery. Integrated metaproteomic and metabolomic analyses revealed functional reprogramming of the microbiota, characterized by upregulation of vitamin and cofactor biosynthesis, nutrient acquisition, and detoxification pathways, and decreased carbohydrate fermentation and amino acid turnover, consistent with reduced short-chain fatty acid levels. Microbiome-depleted and SIHUMIx-inoculated larvae were exposed to azoxystrobin at 4 days post fertilization and neurobehavioral outcomes were assessed after 24 h using the Visual and Acoustic Motor Response assay. Azoxystrobin exposure disrupted non-associative habituation learning independent of microbiome status but induced dark phase-hyperactivity only in colonized larvae, indicating a microbiome-dependent phenotype. Targeted metabolomics revealed lower serotonin levels in microbiome-depleted larvae relative to colonized controls, and that azoxystrobin exposure reduced serotonin in colonized larvae toward depleted levels. These results suggest that microbiota-dependent serotonergic signaling may modulate host responses to azoxystrobin. This integrated ex vivo-in vivo approach supports the concept that the microbiome is a key determinant of neurotoxic responses and underscores the importance of incorporating microbiome-mediated effects into chemical risk assessment frameworks.
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@article {pmid41795836,
year = {2026},
author = {Wray, C and Castañeda-Monsalve, V and Engelmann, B and Rolle-Kampczyk, UE and Schweiger, N and Gutsfeld, S and Ghosh, D and Kader, S and Tyler, CR and Jehmlich, N and Tal, T},
title = {Integration of human microbiota (SIHUMIx) and zebrafish models reveals microbiome-mediated host responses to azoxystrobin.},
journal = {Toxicological sciences : an official journal of the Society of Toxicology},
volume = {},
number = {},
pages = {},
doi = {10.1093/toxsci/kfag022},
pmid = {41795836},
issn = {1096-0929},
abstract = {The gut microbiome is essential for neurodevelopment via bidirectional gut-brain axis signaling, yet environmental chemicals can potentially disrupt this communication by altering community structure and xenobiotic metabolism. In this study, we investigated whether the fungicide azoxystrobin, a known metabolic disruptor, modulates microbiome composition and function to influence neurobehavior. We utilized a simplified human gut microbiota model (SIHUMIx) and a vertebrate host model (larval zebrafish) to elucidate microbiome-mediated mechanisms of xenobiotic neurotoxicity. SIHUMIx was exposed to azoxystrobin for 7 days at 10% of the acceptable daily intake, followed by recovery. Integrated metaproteomic and metabolomic analyses revealed functional reprogramming of the microbiota, characterized by upregulation of vitamin and cofactor biosynthesis, nutrient acquisition, and detoxification pathways, and decreased carbohydrate fermentation and amino acid turnover, consistent with reduced short-chain fatty acid levels. Microbiome-depleted and SIHUMIx-inoculated larvae were exposed to azoxystrobin at 4 days post fertilization and neurobehavioral outcomes were assessed after 24 h using the Visual and Acoustic Motor Response assay. Azoxystrobin exposure disrupted non-associative habituation learning independent of microbiome status but induced dark phase-hyperactivity only in colonized larvae, indicating a microbiome-dependent phenotype. Targeted metabolomics revealed lower serotonin levels in microbiome-depleted larvae relative to colonized controls, and that azoxystrobin exposure reduced serotonin in colonized larvae toward depleted levels. These results suggest that microbiota-dependent serotonergic signaling may modulate host responses to azoxystrobin. This integrated ex vivo-in vivo approach supports the concept that the microbiome is a key determinant of neurotoxic responses and underscores the importance of incorporating microbiome-mediated effects into chemical risk assessment frameworks.},
}
RevDate: 2026-03-08
Microbial dynamics in sorghum-based diets: impact of phase feeding and phytase superdosing vs. corn-based diets.
Research in veterinary science, 204:106130 pii:S0034-5288(26)00082-2 [Epub ahead of print].
This study evaluated the cecal microbiome of broilers fed sorghum- or corn-based diets with standard or superdosed phytase across different feeding phases. A total of 1500 male broiler chicks were reared for 42 days in a floor pen facility and assigned to three dietary treatments. Birds received a corn-based diet with standard phytase, a sorghum-based diet with standard phytase, or a sorghum-based diet with phytase superdosing. Cecal samples were collected at the end of the starter, grower, and finisher phases for 16S rRNA sequencing. Microbial diversity increased as birds matured, with the lowest diversity observed in the starter phase and the greatest richness in the finisher phase. Microbial community structure clustered distinctly by feeding phase, confirming that age and diet progression were the main drivers of microbiota composition. Grain type and phytase level had minimal influence on alpha or beta diversity, although sorghum inclusion was associated with shifts in specific taxa, such as increased Muribaculaceae and reduced Ruminococcaceae. Overall growth performance and microbiome profiles were similar across dietary treatments, reinforcing the potential of sorghum as an effective substitute for corn in broiler diets. The findings highlight the importance of diet phase progression in shaping gut microbial communities and demonstrate that phytase superdosing does not substantially alter microbiome dynamics under these conditions.
Additional Links: PMID-41795238
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@article {pmid41795238,
year = {2026},
author = {Sasia, S and Ortiz, M and Peña, M and Lumpkins, B and Arguelles-Ramos, M},
title = {Microbial dynamics in sorghum-based diets: impact of phase feeding and phytase superdosing vs. corn-based diets.},
journal = {Research in veterinary science},
volume = {204},
number = {},
pages = {106130},
doi = {10.1016/j.rvsc.2026.106130},
pmid = {41795238},
issn = {1532-2661},
abstract = {This study evaluated the cecal microbiome of broilers fed sorghum- or corn-based diets with standard or superdosed phytase across different feeding phases. A total of 1500 male broiler chicks were reared for 42 days in a floor pen facility and assigned to three dietary treatments. Birds received a corn-based diet with standard phytase, a sorghum-based diet with standard phytase, or a sorghum-based diet with phytase superdosing. Cecal samples were collected at the end of the starter, grower, and finisher phases for 16S rRNA sequencing. Microbial diversity increased as birds matured, with the lowest diversity observed in the starter phase and the greatest richness in the finisher phase. Microbial community structure clustered distinctly by feeding phase, confirming that age and diet progression were the main drivers of microbiota composition. Grain type and phytase level had minimal influence on alpha or beta diversity, although sorghum inclusion was associated with shifts in specific taxa, such as increased Muribaculaceae and reduced Ruminococcaceae. Overall growth performance and microbiome profiles were similar across dietary treatments, reinforcing the potential of sorghum as an effective substitute for corn in broiler diets. The findings highlight the importance of diet phase progression in shaping gut microbial communities and demonstrate that phytase superdosing does not substantially alter microbiome dynamics under these conditions.},
}
RevDate: 2026-03-08
The microbiome research in obstetrics and gynecology is getting attention-Some reasons why.
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@article {pmid41795148,
year = {2026},
author = {Shabana, H and Rodriguez-Wallberg, KA},
title = {The microbiome research in obstetrics and gynecology is getting attention-Some reasons why.},
journal = {Acta obstetricia et gynecologica Scandinavica},
volume = {},
number = {},
pages = {},
doi = {10.1111/aogs.70184},
pmid = {41795148},
issn = {1600-0412},
}
RevDate: 2026-03-07
CmpDate: 2026-03-08
Interactions of Mucus Monosaccharides and the Epidermal Microbiome in Four Benthic Elasmobranchs.
Environmental microbiology reports, 18(2):e70303.
Epidermal mucus is a complicated mixture of macromolecules which acts as the first line of defence for organisms against abrasions and infections. We quantified the carbohydrate (monosaccharide) composition of the mucus from four Elasmobranchii hosts, including eagle rays (Myliobatis tenuicaudatus), Port Jackson sharks (Heterodontus portusjacksoni), Australian angelsharks (Squatina australis) and whitespotted skates (Dentiraja cerva). Elasmobranchii had low amounts of mucus and a low proportion of carbohydrates (< 10%) compared with other marine organisms. Four key monosaccharides: glucose, glucosamine, galactose and fucose, were identified in mucus samples. Hosts exhibited distinct, species-specific monosaccharide signatures. We identified key carbohydrate microbial genes from host and water microbiomes. Elasmobranch microbiomes had a higher relative abundance of carbon utilisation genes compared to the water column and contained gene pathways for the utilisation of specific monosaccharides found in host mucus, suggesting that the host mucus was a regulator of the microbiome. Elasmobranch epidermal microbiomes have the genetic machinery required for detecting, transporting and metabolising monosaccharides and other carbohydrates present in the host mucus, demonstrating the selective nature of Elasmobranch epidermal mucus.
Additional Links: PMID-41795122
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@article {pmid41795122,
year = {2026},
author = {Kerr, EN and Yu, L and Hesse, RD and Roberts, CN and Bulone, V and Meyer, L and Edwards, RA and Doane, MP and Dinsdale, EA},
title = {Interactions of Mucus Monosaccharides and the Epidermal Microbiome in Four Benthic Elasmobranchs.},
journal = {Environmental microbiology reports},
volume = {18},
number = {2},
pages = {e70303},
pmid = {41795122},
issn = {1758-2229},
support = {//Royal Society for South Australia/ ; RC2DK116713/NH/NIH HHS/United States ; DP220102915//Australian Research Council/ ; },
mesh = {Animals ; *Mucus/chemistry/metabolism/microbiology ; *Monosaccharides/metabolism/analysis ; *Microbiota ; *Epidermis/microbiology ; *Elasmobranchii/microbiology/metabolism ; Bacteria/genetics/classification/metabolism/isolation & purification ; Skin Microbiome ; },
abstract = {Epidermal mucus is a complicated mixture of macromolecules which acts as the first line of defence for organisms against abrasions and infections. We quantified the carbohydrate (monosaccharide) composition of the mucus from four Elasmobranchii hosts, including eagle rays (Myliobatis tenuicaudatus), Port Jackson sharks (Heterodontus portusjacksoni), Australian angelsharks (Squatina australis) and whitespotted skates (Dentiraja cerva). Elasmobranchii had low amounts of mucus and a low proportion of carbohydrates (< 10%) compared with other marine organisms. Four key monosaccharides: glucose, glucosamine, galactose and fucose, were identified in mucus samples. Hosts exhibited distinct, species-specific monosaccharide signatures. We identified key carbohydrate microbial genes from host and water microbiomes. Elasmobranch microbiomes had a higher relative abundance of carbon utilisation genes compared to the water column and contained gene pathways for the utilisation of specific monosaccharides found in host mucus, suggesting that the host mucus was a regulator of the microbiome. Elasmobranch epidermal microbiomes have the genetic machinery required for detecting, transporting and metabolising monosaccharides and other carbohydrates present in the host mucus, demonstrating the selective nature of Elasmobranch epidermal mucus.},
}
MeSH Terms:
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Animals
*Mucus/chemistry/metabolism/microbiology
*Monosaccharides/metabolism/analysis
*Microbiota
*Epidermis/microbiology
*Elasmobranchii/microbiology/metabolism
Bacteria/genetics/classification/metabolism/isolation & purification
Skin Microbiome
RevDate: 2026-03-07
Soil acidification dismantles a citrulline-mediated microbe-metabolite-host defense axis in watermelon, exacerbating Fusarium wilt.
NPJ biofilms and microbiomes pii:10.1038/s41522-026-00951-7 [Epub ahead of print].
Soil acidification disrupts the structure and function of soil microbiomes, resulting in increased vulnerability to soil-borne pathogens. While the link between soil acidification and disease susceptibility is well-established, the mechanisms underlying the suppression of plant defense remain poorly understood. In this study, we found that soil acidification perturbed the co-evolved assembly process of endophytic microbiomes in watermelon roots, leading to the collapse of a critical microbe-metabolite-host defense axis essential for resistance against Fusarium oxysporum f. sp. niveum (FON). Integrated field surveys and multi-omics analyses revealed that acidification-induced dysbiosis in the root endophytic microbiomes, characterized by the depletion of keystone Pseudomonas species (Pseudomonadaceae), strongly correlated with increased Fusarium wilt incidence. Central to this interaction was citrulline, a metabolite produced by root Pseudomonas endophytes that functioned as a symbiotic effector promoting bacterial colonization and a defense modulator inhibiting FON-induced oxidative burst. Disruption of citrulline biosynthesis abolished these protective effects, whereas exogenous citrulline application restored disease resistance. These findings underscored the role of root endophyte-derived citrulline in sustaining microbial fitness and plant defense, revealing a tripartite interaction impacted by soil acidification. Collectively, this study provides insights for developing microbiome-based strategies to enhance sustainable crop protection in degraded agroecosystems.
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@article {pmid41794853,
year = {2026},
author = {Zhang, Z and Yu, L and Wu, C and Guo, J and Zhu, L and Wang, J and Zhou, C},
title = {Soil acidification dismantles a citrulline-mediated microbe-metabolite-host defense axis in watermelon, exacerbating Fusarium wilt.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-00951-7},
pmid = {41794853},
issn = {2055-5008},
support = {20250586//where they are referenced/ ; 2023AH020024, gxyq2022053//Natural Science Foundation of Universities in Anhui Province/ ; XK-XJGY003//University-Level Advanced Discipline/ ; DTR2024033//Discipline (Major) Leader Development Program/ ; },
abstract = {Soil acidification disrupts the structure and function of soil microbiomes, resulting in increased vulnerability to soil-borne pathogens. While the link between soil acidification and disease susceptibility is well-established, the mechanisms underlying the suppression of plant defense remain poorly understood. In this study, we found that soil acidification perturbed the co-evolved assembly process of endophytic microbiomes in watermelon roots, leading to the collapse of a critical microbe-metabolite-host defense axis essential for resistance against Fusarium oxysporum f. sp. niveum (FON). Integrated field surveys and multi-omics analyses revealed that acidification-induced dysbiosis in the root endophytic microbiomes, characterized by the depletion of keystone Pseudomonas species (Pseudomonadaceae), strongly correlated with increased Fusarium wilt incidence. Central to this interaction was citrulline, a metabolite produced by root Pseudomonas endophytes that functioned as a symbiotic effector promoting bacterial colonization and a defense modulator inhibiting FON-induced oxidative burst. Disruption of citrulline biosynthesis abolished these protective effects, whereas exogenous citrulline application restored disease resistance. These findings underscored the role of root endophyte-derived citrulline in sustaining microbial fitness and plant defense, revealing a tripartite interaction impacted by soil acidification. Collectively, this study provides insights for developing microbiome-based strategies to enhance sustainable crop protection in degraded agroecosystems.},
}
RevDate: 2026-03-07
The hydrocarbon-degrading bacteria and fungi in oil contaminated soils of Kazakhstan: microbiome composition, enrichment, isolation and bioremediation potential.
Environmental microbiome pii:10.1186/s40793-026-00866-y [Epub ahead of print].
BACKGROUND: Oil contamination in soils causes significant environmental impacts and risks to human health. Oil components can be naturally reduced by indigenous microorganisms, that are able to degrade such substrates. We used culture-independent and culture-dependent methods to examine the prokaryotic and the eukaryotic microbiome of different heavily oil contaminated soils in Kazakhstan. Bacteria and fungi were enriched and isolated from four soils contaminated with crude oil or hydrocarbons. Aliphatic, aromatic and condensed aromatic model hydrocarbons of crude oil and crude oil itself were used as substrates for the enrichment and the isolation experiments. The enrichment process was accompanied by culture-independent tests.
RESULTS: The results of the Illumina sequencing of the contaminated soils and the enrichment cultures were compared with the results of the culture-dependent isolation and determination of bacterial, yeast and filamentous fungal strains. The majority of these 110 strains from 45 different genera belong to well-described hydrocarbon degraders like Bacilli and Rhodococci as well as to Achromobacter, Gordonia, Pseudomonas, Stenotrophomonas, Aspergillus, Exophiala, Fusarium, Meyerozyma, Penicillium and Trichoderma species. The most abundant species was the ascomycetal yeast Meyerozyma guilliermondii followed by strains of the bacterial genus Peribacillus. Furthermore, we combined the microbiome insights on the enrichment procedures and the isolation of bacteria, yeasts and filamentous fungi with the in-fact degradation potential of the isolated species based on substrate consumption and metabolite formation. In addition to the well-described hydrocarbon degraders, the utilization spectrum of less-studied strains of the genera Leifsonia, Neorhizobium, Purpureocillium, Rhodotorula and Sarocladium could be broadened.
CONCLUSION: In the end a complex overview of the indigenous microorganisms and their degradation ability of crude oil components emerged and demonstrates the great potential of bioremediation for Kazakhstan soils.
Additional Links: PMID-41794812
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@article {pmid41794812,
year = {2026},
author = {Müller, F and Wang, H and Reinhard, A and Omirbekova, A and Berzhanova, R and Mukasheva, T and Urich, T and Mikolasch, A},
title = {The hydrocarbon-degrading bacteria and fungi in oil contaminated soils of Kazakhstan: microbiome composition, enrichment, isolation and bioremediation potential.},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-026-00866-y},
pmid = {41794812},
issn = {2524-6372},
abstract = {BACKGROUND: Oil contamination in soils causes significant environmental impacts and risks to human health. Oil components can be naturally reduced by indigenous microorganisms, that are able to degrade such substrates. We used culture-independent and culture-dependent methods to examine the prokaryotic and the eukaryotic microbiome of different heavily oil contaminated soils in Kazakhstan. Bacteria and fungi were enriched and isolated from four soils contaminated with crude oil or hydrocarbons. Aliphatic, aromatic and condensed aromatic model hydrocarbons of crude oil and crude oil itself were used as substrates for the enrichment and the isolation experiments. The enrichment process was accompanied by culture-independent tests.
RESULTS: The results of the Illumina sequencing of the contaminated soils and the enrichment cultures were compared with the results of the culture-dependent isolation and determination of bacterial, yeast and filamentous fungal strains. The majority of these 110 strains from 45 different genera belong to well-described hydrocarbon degraders like Bacilli and Rhodococci as well as to Achromobacter, Gordonia, Pseudomonas, Stenotrophomonas, Aspergillus, Exophiala, Fusarium, Meyerozyma, Penicillium and Trichoderma species. The most abundant species was the ascomycetal yeast Meyerozyma guilliermondii followed by strains of the bacterial genus Peribacillus. Furthermore, we combined the microbiome insights on the enrichment procedures and the isolation of bacteria, yeasts and filamentous fungi with the in-fact degradation potential of the isolated species based on substrate consumption and metabolite formation. In addition to the well-described hydrocarbon degraders, the utilization spectrum of less-studied strains of the genera Leifsonia, Neorhizobium, Purpureocillium, Rhodotorula and Sarocladium could be broadened.
CONCLUSION: In the end a complex overview of the indigenous microorganisms and their degradation ability of crude oil components emerged and demonstrates the great potential of bioremediation for Kazakhstan soils.},
}
RevDate: 2026-03-07
Characterisation of the wound microbiome and antimicrobial resistance profiles in clinical isolates from epidermolysis bullosa patients.
Orphanet journal of rare diseases pii:10.1186/s13023-026-04295-5 [Epub ahead of print].
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@article {pmid41794696,
year = {2026},
author = {Amsalu, A and Haidari, H and Mirco, B and Rudolph-Stringer, V and Walter, S and Antipov, A and Murrell, DF and Kopecki, Z},
title = {Characterisation of the wound microbiome and antimicrobial resistance profiles in clinical isolates from epidermolysis bullosa patients.},
journal = {Orphanet journal of rare diseases},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13023-026-04295-5},
pmid = {41794696},
issn = {1750-1172},
support = {Channel 7 Children's Research Foundation//Channel 7 Children's Research Foundation/ ; DEBRA Australia//DEBRA Australia/ ; Epidermolysis Bullosa Medical Research Foundation//Epidermolysis Bullosa Medical Research Foundation/ ; },
}
RevDate: 2026-03-07
Corrigendum to "Environmentally relevant levels of sulfamethoxazole (SMX) alter the skin and gastrointestinal microbiome of adult male and female zebrafish (Danio rerio)" [Aquatic Toxicology, Volume 288 (2025) 107546].
Additional Links: PMID-41794620
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@article {pmid41794620,
year = {2026},
author = {Iftikhar, N and Konig, I and Brammer-Robbins, E and Kozuch, M and Bisesi, JH and Hashmi, I and Martyniuk, CJ},
title = {Corrigendum to "Environmentally relevant levels of sulfamethoxazole (SMX) alter the skin and gastrointestinal microbiome of adult male and female zebrafish (Danio rerio)" [Aquatic Toxicology, Volume 288 (2025) 107546].},
journal = {Aquatic toxicology (Amsterdam, Netherlands)},
volume = {},
number = {},
pages = {107767},
doi = {10.1016/j.aquatox.2026.107767},
pmid = {41794620},
issn = {1879-1514},
}
RevDate: 2026-03-07
CmpDate: 2026-03-07
ILA-producing bifidobacterium bifidum ameliorates chronic kidney disease via AHR signaling by modulating the gut-kidney axis.
Food research international (Ottawa, Ont.), 230:118638.
Chronic kidney disease (CKD) is associated with gut microbiota dysbiosis and disruption of the gut-kidney axis, making probiotics-which can modulate host metabolism and the gut microbiome-a highly promising intervention strategy. Building on this premise, this study used High-Performance Liquid Chromatography (HPLC) to screen 39 candidate strains and successfully isolate two high indole-3-lactic acid (ILA)-producing strains of Bifidobacterium bifidum: FL228.1 and ZL.1. Whole-genome sequencing subsequently confirmed that both strains possess the aromatic lactate dehydrogenase (Aldh) gene, which is essential for ILA biosynthesis. The strains were then evaluated in an adenine-induced CKD mouse model. ZL.1 exhibited pronounced efficacy: it not only improved renal injury, restored gut barrier function, and corrected dysbiosis, as evidenced by an increased relative abundance of Muribaculaceae and a decreased abundance of Dubosiella, but also significantly elevated the level of the key metabolite ILA. In-depth mechanistic analysis revealed that ILA exerts its effects by activating the aryl hydrocarbon receptor (AHR) signaling pathway, which in turn inhibits NLRP3 inflammasome activation, thereby achieving the dual benefit of mitigating intestinal inflammation and alleviating renal fibrosis. Targeted metabolomics analysis supported the conclusion that high ILA production is a critical characteristic for B. bifidum's modulation of the gut-kidney axis. In contrast, the FL228.1 strain showed moderate effects, with its specific mechanism remaining unclear. In conclusion, our study suggests that ILA-producing B. bifidum may ameliorate CKD by regulating the gut-kidney axis via ILA and AHR signaling. This indicates a potential probiotic strategy targeting tryptophan metabolism for CKD.
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@article {pmid41794500,
year = {2026},
author = {Hua, Q and Meng, Y and Hu, J and Wei, Y and Yi, H and Liang, X and Zhang, L and Zhang, Z},
title = {ILA-producing bifidobacterium bifidum ameliorates chronic kidney disease via AHR signaling by modulating the gut-kidney axis.},
journal = {Food research international (Ottawa, Ont.)},
volume = {230},
number = {},
pages = {118638},
doi = {10.1016/j.foodres.2026.118638},
pmid = {41794500},
issn = {1873-7145},
mesh = {Animals ; *Renal Insufficiency, Chronic/therapy/microbiology/metabolism ; *Receptors, Aryl Hydrocarbon/metabolism ; *Gastrointestinal Microbiome ; Signal Transduction ; Mice ; *Probiotics/pharmacology ; *Bifidobacterium bifidum/metabolism/genetics ; *Indoles/metabolism ; Kidney/metabolism ; Male ; Disease Models, Animal ; *Lactic Acid/metabolism/analogs & derivatives ; Dysbiosis ; Mice, Inbred C57BL ; *Basic Helix-Loop-Helix Proteins/metabolism ; },
abstract = {Chronic kidney disease (CKD) is associated with gut microbiota dysbiosis and disruption of the gut-kidney axis, making probiotics-which can modulate host metabolism and the gut microbiome-a highly promising intervention strategy. Building on this premise, this study used High-Performance Liquid Chromatography (HPLC) to screen 39 candidate strains and successfully isolate two high indole-3-lactic acid (ILA)-producing strains of Bifidobacterium bifidum: FL228.1 and ZL.1. Whole-genome sequencing subsequently confirmed that both strains possess the aromatic lactate dehydrogenase (Aldh) gene, which is essential for ILA biosynthesis. The strains were then evaluated in an adenine-induced CKD mouse model. ZL.1 exhibited pronounced efficacy: it not only improved renal injury, restored gut barrier function, and corrected dysbiosis, as evidenced by an increased relative abundance of Muribaculaceae and a decreased abundance of Dubosiella, but also significantly elevated the level of the key metabolite ILA. In-depth mechanistic analysis revealed that ILA exerts its effects by activating the aryl hydrocarbon receptor (AHR) signaling pathway, which in turn inhibits NLRP3 inflammasome activation, thereby achieving the dual benefit of mitigating intestinal inflammation and alleviating renal fibrosis. Targeted metabolomics analysis supported the conclusion that high ILA production is a critical characteristic for B. bifidum's modulation of the gut-kidney axis. In contrast, the FL228.1 strain showed moderate effects, with its specific mechanism remaining unclear. In conclusion, our study suggests that ILA-producing B. bifidum may ameliorate CKD by regulating the gut-kidney axis via ILA and AHR signaling. This indicates a potential probiotic strategy targeting tryptophan metabolism for CKD.},
}
MeSH Terms:
show MeSH Terms
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Animals
*Renal Insufficiency, Chronic/therapy/microbiology/metabolism
*Receptors, Aryl Hydrocarbon/metabolism
*Gastrointestinal Microbiome
Signal Transduction
Mice
*Probiotics/pharmacology
*Bifidobacterium bifidum/metabolism/genetics
*Indoles/metabolism
Kidney/metabolism
Male
Disease Models, Animal
*Lactic Acid/metabolism/analogs & derivatives
Dysbiosis
Mice, Inbred C57BL
*Basic Helix-Loop-Helix Proteins/metabolism
RevDate: 2026-03-07
CmpDate: 2026-03-07
Interplay of probiotics, prebiotics, synbiotics and postbiotics: a review of their therapeutic potential for gastrointestinal inflammation.
Food research international (Ottawa, Ont.), 230:118598.
Gastrointestinal inflammation is a multifaceted condition deeply connected to the gut microbiota. The prebiotics, probiotics, synbiotics and their metabolites, termed postbiotics, have been explored extensively in the past as a novel approach in managing inflammatory bowel disorders. Prebiotics, probiotics, and postbiotics derived from food sources play crucial roles in modulating the gut microbiota and significantly impact gastrointestinal inflammation. Prebiotics are non-digestible, selectively fermented dietary fibers found in foods such as inulin-type fructans and galacto-oligosaccharides that promote the growth of beneficial gut bacteria like bifidobacteria and lactobacilli. These prebiotics contribute to the production of short-chain fatty acids which possess anti-inflammatory properties and enhance immune regulation in the gut. Together, prebiotics, probiotics, and postbiotics synergistically maintain and restore gastrointestinal health by modulating the gut microbiome composition, enhancing production of anti-inflammatory metabolites, strengthening the intestinal barrier, and regulating immune responses. These interventions show promise in preventing and managing gastrointestinal inflammatory conditions such as irritable bowel syndrome, Crohn's disease, and ulcerative colitis by counteracting dysbiosis and mucosal inflammation. Drawing from recent preclinical and clinical studies, these strategies have shown promising results in managing gastrointestinal inflammation. Despite the compelling evidence, significant challenges remain. These include the considerable variability of host responses, the necessity for standardized strains and precise dosages, and a lack of a unified regulatory framework. This comprehensive review integrates the current understanding of prebiotics, probiotics, synbiotics, and postbiotics, highlighting their mechanistic interplay and highly promising role in managing gastrointestinal inflammation. It provides an in-depth discussion on current limitations and future directions for research and clinical application.
Additional Links: PMID-41794479
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PubMed:
Citation:
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@article {pmid41794479,
year = {2026},
author = {Baheti, R and Deshkar, S and Jadhav, S and Mule, K and Jha, A and Giram, P and Mahore, J},
title = {Interplay of probiotics, prebiotics, synbiotics and postbiotics: a review of their therapeutic potential for gastrointestinal inflammation.},
journal = {Food research international (Ottawa, Ont.)},
volume = {230},
number = {},
pages = {118598},
doi = {10.1016/j.foodres.2026.118598},
pmid = {41794479},
issn = {1873-7145},
mesh = {*Prebiotics/administration & dosage ; Humans ; *Probiotics/therapeutic use/administration & dosage ; *Synbiotics/administration & dosage ; Gastrointestinal Microbiome ; Animals ; *Inflammation ; *Inflammatory Bowel Diseases/microbiology/therapy ; *Gastrointestinal Diseases/therapy ; },
abstract = {Gastrointestinal inflammation is a multifaceted condition deeply connected to the gut microbiota. The prebiotics, probiotics, synbiotics and their metabolites, termed postbiotics, have been explored extensively in the past as a novel approach in managing inflammatory bowel disorders. Prebiotics, probiotics, and postbiotics derived from food sources play crucial roles in modulating the gut microbiota and significantly impact gastrointestinal inflammation. Prebiotics are non-digestible, selectively fermented dietary fibers found in foods such as inulin-type fructans and galacto-oligosaccharides that promote the growth of beneficial gut bacteria like bifidobacteria and lactobacilli. These prebiotics contribute to the production of short-chain fatty acids which possess anti-inflammatory properties and enhance immune regulation in the gut. Together, prebiotics, probiotics, and postbiotics synergistically maintain and restore gastrointestinal health by modulating the gut microbiome composition, enhancing production of anti-inflammatory metabolites, strengthening the intestinal barrier, and regulating immune responses. These interventions show promise in preventing and managing gastrointestinal inflammatory conditions such as irritable bowel syndrome, Crohn's disease, and ulcerative colitis by counteracting dysbiosis and mucosal inflammation. Drawing from recent preclinical and clinical studies, these strategies have shown promising results in managing gastrointestinal inflammation. Despite the compelling evidence, significant challenges remain. These include the considerable variability of host responses, the necessity for standardized strains and precise dosages, and a lack of a unified regulatory framework. This comprehensive review integrates the current understanding of prebiotics, probiotics, synbiotics, and postbiotics, highlighting their mechanistic interplay and highly promising role in managing gastrointestinal inflammation. It provides an in-depth discussion on current limitations and future directions for research and clinical application.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Prebiotics/administration & dosage
Humans
*Probiotics/therapeutic use/administration & dosage
*Synbiotics/administration & dosage
Gastrointestinal Microbiome
Animals
*Inflammation
*Inflammatory Bowel Diseases/microbiology/therapy
*Gastrointestinal Diseases/therapy
RevDate: 2026-03-07
CmpDate: 2026-03-07
Kombucha meets circular economy: A microbiome and metabolite perspective on second fermentation with plant by-products.
Food research international (Ottawa, Ont.), 230:118597.
Kombucha is a traditional fermented beverage produced through the fermentation of sugared tea by a symbiotic culture of bacteria and yeasts (SCOBY). In recent years, the valorisation of plant-based by-products as fermentation substrates has gained attention as a sustainable approach to improving both the nutritional and economic efficiency of fermented beverages. The present study investigated the production of kombuchas supplemented with pineapple, fennel, and carrot by-products during the secondary fermentation phase, aiming to evaluate their influence on fermentation dynamics, microbial ecology, and the chemical and aromatic profiles of the final products. The experimental design integrated culture-dependent and culture-independent approaches, including amplicon sequencing, to characterize microbial community composition and evolution throughout fermentation. Chemical profiling was carried out using gas chromatography coupled with quadrupole mass spectrometry (GC-qMS) and high-performance liquid chromatography equipped with diode-array and refractive index detectors (HPLC-DAD/RI). The fermentation process was monitored during both the primary and secondary stages, and a shelf-life assessment was conducted over 14 days of refrigerated storage (4 °C) to evaluate product stability. Microbiological results indicated a predominance of Schizosaccharomyces spp., while Komagataeibacter spp. was the only bacterial genus identified. A significant reduction in α-diversity was observed over time, suggesting selective adaptation of the microbial community to the fermentation environment. β-diversity analysis revealed clear differences among samples collected after 8 and 22 days, reflecting the combined influence of time and substrate composition on microbial succession. Chemical analyses demonstrated an increase in acetic acid concentration and a progressive decline in pH throughout fermentation, consistent with the metabolic activity of acetic acid bacteria. Among volatile organic compounds (VOCs), alcohols and organic acids were the most abundant chemical classes detected. Several VOCs were associated with minor yeast genera, including Hannaella, Galactomyces, Aureobasidium, and Millerozyma, whereas Schizosaccharomyces spp. showed a strong correlation with specific aroma-active compounds, highlighting its key role in defining the sensory characteristics of the beverage. Overall, this study provides new evidence on how different vegetable by-products and microbial consortia influence the development of chemical and aromatic compounds in kombucha. The findings highlight the potential of using by-products as a sustainable, value-added strategy for producing fermented beverages, while also supporting the principles of the circular economy and resource-efficient food systems.
Additional Links: PMID-41794478
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PubMed:
Citation:
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@article {pmid41794478,
year = {2026},
author = {Chiarini, E and Buzzanca, D and Devizia, A and Giordano, M and Dipietro, F and Zeppa, G and Alessandria, V},
title = {Kombucha meets circular economy: A microbiome and metabolite perspective on second fermentation with plant by-products.},
journal = {Food research international (Ottawa, Ont.)},
volume = {230},
number = {},
pages = {118597},
doi = {10.1016/j.foodres.2026.118597},
pmid = {41794478},
issn = {1873-7145},
mesh = {*Fermentation ; *Microbiota ; *Kombucha Tea/microbiology/analysis/economics ; Food Microbiology ; Bacteria/metabolism/classification ; Yeasts/metabolism ; Volatile Organic Compounds/analysis ; Gas Chromatography-Mass Spectrometry ; },
abstract = {Kombucha is a traditional fermented beverage produced through the fermentation of sugared tea by a symbiotic culture of bacteria and yeasts (SCOBY). In recent years, the valorisation of plant-based by-products as fermentation substrates has gained attention as a sustainable approach to improving both the nutritional and economic efficiency of fermented beverages. The present study investigated the production of kombuchas supplemented with pineapple, fennel, and carrot by-products during the secondary fermentation phase, aiming to evaluate their influence on fermentation dynamics, microbial ecology, and the chemical and aromatic profiles of the final products. The experimental design integrated culture-dependent and culture-independent approaches, including amplicon sequencing, to characterize microbial community composition and evolution throughout fermentation. Chemical profiling was carried out using gas chromatography coupled with quadrupole mass spectrometry (GC-qMS) and high-performance liquid chromatography equipped with diode-array and refractive index detectors (HPLC-DAD/RI). The fermentation process was monitored during both the primary and secondary stages, and a shelf-life assessment was conducted over 14 days of refrigerated storage (4 °C) to evaluate product stability. Microbiological results indicated a predominance of Schizosaccharomyces spp., while Komagataeibacter spp. was the only bacterial genus identified. A significant reduction in α-diversity was observed over time, suggesting selective adaptation of the microbial community to the fermentation environment. β-diversity analysis revealed clear differences among samples collected after 8 and 22 days, reflecting the combined influence of time and substrate composition on microbial succession. Chemical analyses demonstrated an increase in acetic acid concentration and a progressive decline in pH throughout fermentation, consistent with the metabolic activity of acetic acid bacteria. Among volatile organic compounds (VOCs), alcohols and organic acids were the most abundant chemical classes detected. Several VOCs were associated with minor yeast genera, including Hannaella, Galactomyces, Aureobasidium, and Millerozyma, whereas Schizosaccharomyces spp. showed a strong correlation with specific aroma-active compounds, highlighting its key role in defining the sensory characteristics of the beverage. Overall, this study provides new evidence on how different vegetable by-products and microbial consortia influence the development of chemical and aromatic compounds in kombucha. The findings highlight the potential of using by-products as a sustainable, value-added strategy for producing fermented beverages, while also supporting the principles of the circular economy and resource-efficient food systems.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Fermentation
*Microbiota
*Kombucha Tea/microbiology/analysis/economics
Food Microbiology
Bacteria/metabolism/classification
Yeasts/metabolism
Volatile Organic Compounds/analysis
Gas Chromatography-Mass Spectrometry
RevDate: 2026-03-07
CmpDate: 2026-03-07
Alpha-lipoic acid improves intestinal homeostasis and ameliorates colitis through modulation of gut microbiota and production of short chain fatty acids in mice.
Food research international (Ottawa, Ont.), 230:118582.
α-Lipoic acid (ALA) is a natural antioxidant present in both plants and animal foods. It has attracted growing attention for its potential role in maintenance of intestinal homeostasis. This study was to investigate the protective effects of dietary ALA on experimental colitis, and to evaluate its modulating effect on gut microbiome in mice. Male C57BL/6 J mice with dextran sulfate sodium (DSS)-induced acute colitis were administered ALA (40 or 80 mg/kg) dissolved in corn oil. Results showed that dietary ALA ameliorated colitis severity, improved intestinal barrier integrity, and attenuated inflammation by reducing oxidative stress and suppressing NF-κB pathway activation and pro-inflammatory cytokines expression. Moreover, dietary ALA increased the microbial diversity (Shannon index), reshaped gut microbiota composition by suppressing pathogenic bacteria and promoting beneficial taxa such as Akkermansia, and elevated levels of short chain fatty acids (SCFA). Fecal microbiota transplantation (FMT) further confirmed that ALA could modulate gut microbiota and protect against colitis in mice. In conclusion, ALA could effectively maintain the intestinal homeostasis and ameliorate colitis at least in mice. Such protective effect of ALA in gut health was mediated through modulation of gut microbiota and enhancement of SCFA production.
Additional Links: PMID-41794466
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PubMed:
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@article {pmid41794466,
year = {2026},
author = {Huang, S and Ding, H and Su, Y and Chen, Z and He, W and Chen, ZY and Zhu, H},
title = {Alpha-lipoic acid improves intestinal homeostasis and ameliorates colitis through modulation of gut microbiota and production of short chain fatty acids in mice.},
journal = {Food research international (Ottawa, Ont.)},
volume = {230},
number = {},
pages = {118582},
doi = {10.1016/j.foodres.2026.118582},
pmid = {41794466},
issn = {1873-7145},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Fatty Acids, Volatile/metabolism ; *Thioctic Acid/pharmacology ; *Colitis/chemically induced/drug therapy/microbiology ; Mice, Inbred C57BL ; Male ; *Homeostasis/drug effects ; Mice ; Dextran Sulfate ; Fecal Microbiota Transplantation ; Oxidative Stress/drug effects ; NF-kappa B/metabolism ; Disease Models, Animal ; Antioxidants/pharmacology ; Cytokines/metabolism ; },
abstract = {α-Lipoic acid (ALA) is a natural antioxidant present in both plants and animal foods. It has attracted growing attention for its potential role in maintenance of intestinal homeostasis. This study was to investigate the protective effects of dietary ALA on experimental colitis, and to evaluate its modulating effect on gut microbiome in mice. Male C57BL/6 J mice with dextran sulfate sodium (DSS)-induced acute colitis were administered ALA (40 or 80 mg/kg) dissolved in corn oil. Results showed that dietary ALA ameliorated colitis severity, improved intestinal barrier integrity, and attenuated inflammation by reducing oxidative stress and suppressing NF-κB pathway activation and pro-inflammatory cytokines expression. Moreover, dietary ALA increased the microbial diversity (Shannon index), reshaped gut microbiota composition by suppressing pathogenic bacteria and promoting beneficial taxa such as Akkermansia, and elevated levels of short chain fatty acids (SCFA). Fecal microbiota transplantation (FMT) further confirmed that ALA could modulate gut microbiota and protect against colitis in mice. In conclusion, ALA could effectively maintain the intestinal homeostasis and ameliorate colitis at least in mice. Such protective effect of ALA in gut health was mediated through modulation of gut microbiota and enhancement of SCFA production.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Gastrointestinal Microbiome/drug effects
*Fatty Acids, Volatile/metabolism
*Thioctic Acid/pharmacology
*Colitis/chemically induced/drug therapy/microbiology
Mice, Inbred C57BL
Male
*Homeostasis/drug effects
Mice
Dextran Sulfate
Fecal Microbiota Transplantation
Oxidative Stress/drug effects
NF-kappa B/metabolism
Disease Models, Animal
Antioxidants/pharmacology
Cytokines/metabolism
RevDate: 2026-03-07
CmpDate: 2026-03-08
The role of mycobiome in terroir and during Muscat grapes fermentation unveiled by multi-omic analysis.
Food research international (Ottawa, Ont.), 230:118577.
The wine microbiome is a key determinant in shaping wine terroir. To date, a comprehensive understanding of how microbial signatures influence wine metabolic profile remains poorly understood. To address this, in the present study an integrated shotgun metagenomics and untargeted metabolomic approach was employed to investigate the wine metabolome and connect the composition and functions of microbiomes involved in wine fermentation of Muscat grapes harvested in Italy and Greece. Beta diversity highlighted the dissimilarity between Italian and Greek fungal terroirs. A marked reduction in diversity during fermentation underscored the dominance of the inoculated Saccharomyces cerevisiae starter culture. The LEfSe analysis revealed an enrichment of Torulaspora delbrueckii in Greek samples, while Kluyveromyces marxianus and lactis were more abundant in Italian samples. Functional analysis revealed geographic differences in nucleotide, fatty acids and lysine metabolisms. Significant shifts were observed in energy, carbohydrate, and amino acid metabolisms, reflecting terroir-specific microbial activity. The metabolomics data highlighted regional differences in oligosaccharides, glycosylated phenolics, peptide and amino acid turnover, and central redox metabolites, suggesting divergent microbial responses and metabolic trajectories shaped by terroir and fermentation conditions. Obtained results highlight the effectiveness of this multi-omics approach in identifying product-specific fungal communities and wine metabolite signatures, providing new tools that could be used to ensure wine authenticity and quality control.
Additional Links: PMID-41794462
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PubMed:
Citation:
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@article {pmid41794462,
year = {2026},
author = {Di Gianvito, P and Sáez, V and Dimopoulou, M and Papandreou, C and Francesca, N and Vrhovsek, U and Rantsiou, K and Cocolin, L and Arapitsas, P and Englezos, V},
title = {The role of mycobiome in terroir and during Muscat grapes fermentation unveiled by multi-omic analysis.},
journal = {Food research international (Ottawa, Ont.)},
volume = {230},
number = {},
pages = {118577},
doi = {10.1016/j.foodres.2026.118577},
pmid = {41794462},
issn = {1873-7145},
mesh = {*Fermentation ; *Vitis/microbiology ; *Wine/microbiology/analysis ; *Mycobiome ; Italy ; Metabolomics/methods ; Greece ; Saccharomyces cerevisiae/metabolism ; Metagenomics/methods ; Food Microbiology ; Metabolome ; Kluyveromyces/metabolism ; Multiomics ; },
abstract = {The wine microbiome is a key determinant in shaping wine terroir. To date, a comprehensive understanding of how microbial signatures influence wine metabolic profile remains poorly understood. To address this, in the present study an integrated shotgun metagenomics and untargeted metabolomic approach was employed to investigate the wine metabolome and connect the composition and functions of microbiomes involved in wine fermentation of Muscat grapes harvested in Italy and Greece. Beta diversity highlighted the dissimilarity between Italian and Greek fungal terroirs. A marked reduction in diversity during fermentation underscored the dominance of the inoculated Saccharomyces cerevisiae starter culture. The LEfSe analysis revealed an enrichment of Torulaspora delbrueckii in Greek samples, while Kluyveromyces marxianus and lactis were more abundant in Italian samples. Functional analysis revealed geographic differences in nucleotide, fatty acids and lysine metabolisms. Significant shifts were observed in energy, carbohydrate, and amino acid metabolisms, reflecting terroir-specific microbial activity. The metabolomics data highlighted regional differences in oligosaccharides, glycosylated phenolics, peptide and amino acid turnover, and central redox metabolites, suggesting divergent microbial responses and metabolic trajectories shaped by terroir and fermentation conditions. Obtained results highlight the effectiveness of this multi-omics approach in identifying product-specific fungal communities and wine metabolite signatures, providing new tools that could be used to ensure wine authenticity and quality control.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Fermentation
*Vitis/microbiology
*Wine/microbiology/analysis
*Mycobiome
Italy
Metabolomics/methods
Greece
Saccharomyces cerevisiae/metabolism
Metagenomics/methods
Food Microbiology
Metabolome
Kluyveromyces/metabolism
Multiomics
RevDate: 2026-03-07
Integrated metabolomics and metagenomics analysis identifies a unique signature characterizing metabolic syndrome.
The Journal of nutritional biochemistry pii:S0955-2863(26)00069-0 [Epub ahead of print].
BACKGROUND: Metabolic Syndrome (MetS) presents a global health challenge, characterized by obesity, hypertension, dyslipidemia, and insulin resistance. Despite recognition of the gut microbiome's role in metabolic health, there remains scope for defining association of unique microbes with clinical status. Unique genetic, dietary, and lifestyle factors may influence gut microbial composition and circulating metabolites, and consequently susceptibility to MetS. By identifying specific microbial and metabolomic signatures associated with MetS, we aim to uncover potential targets for reducing the disease burden.
METHODS: We correlate comprehensive clinical parameters with fecal metagenomics and untargeted serum metabolomics to delineate population-specific characteristics from 142 individuals with MetS (N=97) or control (CTRL; N=45).
RESULTS: Microbiome species-level alpha diversity was reduced in MetS compared to CTRL. After adjustment for sex, age, BMI, and intensity of statin usage, we identified 20 MetS-related species. A co-abundant network analysis revealed Eubacterium eligens, enriched in the CTRL population, with the highest node degree. Serum metabolomics identified 106 significantly differentially regulated metabolites. N-arachidonoyl dopamine (NADA), an endocannabinoid implicated in GABAergic signaling, was the most significantly altered, enriched in CTRL and correlated with E. Eligens. sPLS-DA modeling revealed that E. eligens and D. formicigenerans species cluster together with metabolites NADA and tetrahydrocorticosterone (THB), representing defining characteristics distinguishing MetS in this population.
CONCLUSIONS: Our data reveal a distinct multi-omic signature of MetS, characterized by a significant reduction in E. eligens and D. formicigenerans abundance, and in circulating NADA and THB levels.
Additional Links: PMID-41794383
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PubMed:
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@article {pmid41794383,
year = {2026},
author = {Wannaiampikul, S and Lee, B and Chen, J and Prentice, KJ and Ayansola, R and Xu, A and Santosa, S and Pantopoulos, K and Sweeney, G},
title = {Integrated metabolomics and metagenomics analysis identifies a unique signature characterizing metabolic syndrome.},
journal = {The Journal of nutritional biochemistry},
volume = {},
number = {},
pages = {110327},
doi = {10.1016/j.jnutbio.2026.110327},
pmid = {41794383},
issn = {1873-4847},
abstract = {BACKGROUND: Metabolic Syndrome (MetS) presents a global health challenge, characterized by obesity, hypertension, dyslipidemia, and insulin resistance. Despite recognition of the gut microbiome's role in metabolic health, there remains scope for defining association of unique microbes with clinical status. Unique genetic, dietary, and lifestyle factors may influence gut microbial composition and circulating metabolites, and consequently susceptibility to MetS. By identifying specific microbial and metabolomic signatures associated with MetS, we aim to uncover potential targets for reducing the disease burden.
METHODS: We correlate comprehensive clinical parameters with fecal metagenomics and untargeted serum metabolomics to delineate population-specific characteristics from 142 individuals with MetS (N=97) or control (CTRL; N=45).
RESULTS: Microbiome species-level alpha diversity was reduced in MetS compared to CTRL. After adjustment for sex, age, BMI, and intensity of statin usage, we identified 20 MetS-related species. A co-abundant network analysis revealed Eubacterium eligens, enriched in the CTRL population, with the highest node degree. Serum metabolomics identified 106 significantly differentially regulated metabolites. N-arachidonoyl dopamine (NADA), an endocannabinoid implicated in GABAergic signaling, was the most significantly altered, enriched in CTRL and correlated with E. Eligens. sPLS-DA modeling revealed that E. eligens and D. formicigenerans species cluster together with metabolites NADA and tetrahydrocorticosterone (THB), representing defining characteristics distinguishing MetS in this population.
CONCLUSIONS: Our data reveal a distinct multi-omic signature of MetS, characterized by a significant reduction in E. eligens and D. formicigenerans abundance, and in circulating NADA and THB levels.},
}
RevDate: 2026-03-07
Characterization of an NADPH-dependent 17ɑ-hydroxysteroid dehydrogenase encoded by the desF gene from the gut bacterium Clostridium scindens VPI 12708.
The Journal of steroid biochemistry and molecular biology pii:S0960-0760(26)00048-8 [Epub ahead of print].
Epitestosterone (epiT) is the isomer of the androgen testosterone. Historically, the role of epiT has remained unclear. Recently, it has been reported that epiT promotes nuclear androgen receptor (AR)-dependent prostate cancer cell proliferation. The gut bacterium Clostridium scindens VPI 12708 was shown to convert androstenedione (AD) to epiT over three decades ago. The bacterial enzymatic pathways involved in epiT formation have only recently been reported. The desF gene encodes 17α-hydroxysteroid dehydrogenase which converts AD to epiT using NADPH as a cofactor. In this study, we quantitatively characterized DesF kinetic parameters and substrate specificity. The results revealed that the optimal pH for the reductive reaction is 7.0, and for the oxidative reaction it is 7.5 and 8.0. The kinetic analysis showed that for the reductive reaction, the KM was 8.1 ± 1.8µM and the Vmax was 6.4 ± 0.3 µmol·min[-1]·mg[-1]; for the oxidative direction, the KM was 27.3 ± 3.3µM and the Vmax was 7.2 ± 0.3 µmol·min[-1]·mg[-1]. Moreover, the substrate specificity analysis revealed that 11-keto-AD is the most favourable substrate for DesF, and the 17-keto group of 11-keto-AD can be converted to the 17α-hydroxy group. The phylogenetic relation between DesF and other characterized hydroxysteroid dehydrogenases reveals common ancestry with human HSD17B10 and Eggerthella lenta 3β-HSDH. These results are a significant advance in understanding epiT formation by the gut microbiome.
Additional Links: PMID-41794297
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PubMed:
Citation:
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@article {pmid41794297,
year = {2026},
author = {Wang, T and Binion, B and Alves, JMP and Ridlon, JM},
title = {Characterization of an NADPH-dependent 17ɑ-hydroxysteroid dehydrogenase encoded by the desF gene from the gut bacterium Clostridium scindens VPI 12708.},
journal = {The Journal of steroid biochemistry and molecular biology},
volume = {},
number = {},
pages = {106982},
doi = {10.1016/j.jsbmb.2026.106982},
pmid = {41794297},
issn = {1879-1220},
abstract = {Epitestosterone (epiT) is the isomer of the androgen testosterone. Historically, the role of epiT has remained unclear. Recently, it has been reported that epiT promotes nuclear androgen receptor (AR)-dependent prostate cancer cell proliferation. The gut bacterium Clostridium scindens VPI 12708 was shown to convert androstenedione (AD) to epiT over three decades ago. The bacterial enzymatic pathways involved in epiT formation have only recently been reported. The desF gene encodes 17α-hydroxysteroid dehydrogenase which converts AD to epiT using NADPH as a cofactor. In this study, we quantitatively characterized DesF kinetic parameters and substrate specificity. The results revealed that the optimal pH for the reductive reaction is 7.0, and for the oxidative reaction it is 7.5 and 8.0. The kinetic analysis showed that for the reductive reaction, the KM was 8.1 ± 1.8µM and the Vmax was 6.4 ± 0.3 µmol·min[-1]·mg[-1]; for the oxidative direction, the KM was 27.3 ± 3.3µM and the Vmax was 7.2 ± 0.3 µmol·min[-1]·mg[-1]. Moreover, the substrate specificity analysis revealed that 11-keto-AD is the most favourable substrate for DesF, and the 17-keto group of 11-keto-AD can be converted to the 17α-hydroxy group. The phylogenetic relation between DesF and other characterized hydroxysteroid dehydrogenases reveals common ancestry with human HSD17B10 and Eggerthella lenta 3β-HSDH. These results are a significant advance in understanding epiT formation by the gut microbiome.},
}
RevDate: 2026-03-07
Skin commensal Cutibacterium acnes alleviates UVB-induced solar dermatitis via ceramide-mediated TLR4-MyD88-NF-κB.
Free radical biology & medicine pii:S0891-5849(26)00178-4 [Epub ahead of print].
BACKGROUND: The high-altitude environment is characterized by hypobaric hypoxia and intense ultraviolet B (UVB) radiation, contributing to increased incidence of UVB-induced skin injuries, including plateau solar dermatitis (PSD). The role of commensal skin microbiota in mediating photoprotection under such extreme conditions remains poorly understood. This study aimed to identify UVB-protective skin microbiota in high-altitude populations and to elucidate their potential mechanisms in mitigating UVB-induced skin damage.
METHODS: Skin microbiota profiles were analyzed by 16S rRNA gene sequencing in healthy plateau residents and PSD patients. Protective effects were evaluated using a murine model of UVB-induced skin injury and an in vitro UVB-exposed HaCaT keratinocyte model. Integrated transcriptomic, proteomic, and metabolomic analyses were performed to identify candidate bioactive microbial metabolites, followed by functional validation.
RESULTS: Cutibacterium acnes (C. acnes) was significantly enriched in healthy plateau residents compared with PSD patients. Topical application of C. acnes alleviated UVB-induced skin inflammation, collagen degradation, and DNA damage in mice. Multi-omics analyses revealed dysregulation of sphingolipid metabolism following UVB exposure and highlighted bacterial-derived ceramides as candidate protective metabolites. Two representative ceramides, CER2 and CER14, significantly reduced UVB-induced apoptosis, oxidative stress, and DNA damage in keratinocytes. These effects were associated with suppression of TLR4-MyD88-NF-κB signaling activity.
CONCLUSION: This study identifies C. acnes as a commensal bacterium with photoprotective potential against UVB-induced skin damage in high-altitude environments. Ceramide-related lipid metabolites derived from C. acnes contribute to attenuation of UVB-triggered inflammatory signaling and cellular injury, providing new insights into microbiome-based strategies for photoprotection.
Additional Links: PMID-41794153
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PubMed:
Citation:
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@article {pmid41794153,
year = {2026},
author = {Ma, Y and Ni, Z and Zhu, L and Yang, J and Zhang, Y and Liu, W and Wang, R and Sun, Y and Liu, J and Zhang, P and Yu, L and Huangfu, C and Gao, Y and Zhou, W},
title = {Skin commensal Cutibacterium acnes alleviates UVB-induced solar dermatitis via ceramide-mediated TLR4-MyD88-NF-κB.},
journal = {Free radical biology & medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.freeradbiomed.2026.02.074},
pmid = {41794153},
issn = {1873-4596},
abstract = {BACKGROUND: The high-altitude environment is characterized by hypobaric hypoxia and intense ultraviolet B (UVB) radiation, contributing to increased incidence of UVB-induced skin injuries, including plateau solar dermatitis (PSD). The role of commensal skin microbiota in mediating photoprotection under such extreme conditions remains poorly understood. This study aimed to identify UVB-protective skin microbiota in high-altitude populations and to elucidate their potential mechanisms in mitigating UVB-induced skin damage.
METHODS: Skin microbiota profiles were analyzed by 16S rRNA gene sequencing in healthy plateau residents and PSD patients. Protective effects were evaluated using a murine model of UVB-induced skin injury and an in vitro UVB-exposed HaCaT keratinocyte model. Integrated transcriptomic, proteomic, and metabolomic analyses were performed to identify candidate bioactive microbial metabolites, followed by functional validation.
RESULTS: Cutibacterium acnes (C. acnes) was significantly enriched in healthy plateau residents compared with PSD patients. Topical application of C. acnes alleviated UVB-induced skin inflammation, collagen degradation, and DNA damage in mice. Multi-omics analyses revealed dysregulation of sphingolipid metabolism following UVB exposure and highlighted bacterial-derived ceramides as candidate protective metabolites. Two representative ceramides, CER2 and CER14, significantly reduced UVB-induced apoptosis, oxidative stress, and DNA damage in keratinocytes. These effects were associated with suppression of TLR4-MyD88-NF-κB signaling activity.
CONCLUSION: This study identifies C. acnes as a commensal bacterium with photoprotective potential against UVB-induced skin damage in high-altitude environments. Ceramide-related lipid metabolites derived from C. acnes contribute to attenuation of UVB-triggered inflammatory signaling and cellular injury, providing new insights into microbiome-based strategies for photoprotection.},
}
RevDate: 2026-03-07
The dual binding of pantoprazole mitigates ceftriaxone-mediated misfolding of human serum albumin.
Spectrochimica acta. Part A, Molecular and biomolecular spectroscopy, 355:127661 pii:S1386-1425(26)00232-5 [Epub ahead of print].
Proton pump inhibitors (PPIs) like pantoprazole are often prescribed alongside antibiotics to prevent antibiotic-induced gastritis, ulcers, and microbiome disturbances. In this study, we provide the first evidence of pantoprazole's (PTP) distinct protective role in preventing ceftriaxone (CTX) induced structural alterations and aggregation of human serum albumin (HSA). We have found strong binding of pantoprazole at domain-I and domain-III, whereas ceftriaxone binds in domain-II of HSA. The ceftriaxone binding was found to disrupt the tertiary structure of the protein and induces the non-native β-structures without affecting the thermal stability of the protein. Moreover, it was found to promote the thermal-induced formation of protofibrils. However, the addition of pantoprazole in HSA-CTX complex efficiently restored the structural alterations and aggregation reaction. This study highlights a previously unrecognized protective role of PPIs, particularly pantoprazole, in preserving protein structure and aggregation caused by antibiotic overuse.
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@article {pmid41794001,
year = {2026},
author = {Noor, S and Qureshi, A and Parvez, S and Ahmad, B},
title = {The dual binding of pantoprazole mitigates ceftriaxone-mediated misfolding of human serum albumin.},
journal = {Spectrochimica acta. Part A, Molecular and biomolecular spectroscopy},
volume = {355},
number = {},
pages = {127661},
doi = {10.1016/j.saa.2026.127661},
pmid = {41794001},
issn = {1873-3557},
abstract = {Proton pump inhibitors (PPIs) like pantoprazole are often prescribed alongside antibiotics to prevent antibiotic-induced gastritis, ulcers, and microbiome disturbances. In this study, we provide the first evidence of pantoprazole's (PTP) distinct protective role in preventing ceftriaxone (CTX) induced structural alterations and aggregation of human serum albumin (HSA). We have found strong binding of pantoprazole at domain-I and domain-III, whereas ceftriaxone binds in domain-II of HSA. The ceftriaxone binding was found to disrupt the tertiary structure of the protein and induces the non-native β-structures without affecting the thermal stability of the protein. Moreover, it was found to promote the thermal-induced formation of protofibrils. However, the addition of pantoprazole in HSA-CTX complex efficiently restored the structural alterations and aggregation reaction. This study highlights a previously unrecognized protective role of PPIs, particularly pantoprazole, in preserving protein structure and aggregation caused by antibiotic overuse.},
}
RevDate: 2026-03-07
Serological and faecal markers of irritable bowel syndrome: a systematic review and meta-analysis.
EBioMedicine, 126:106198 pii:S2352-3964(26)00080-0 [Epub ahead of print].
BACKGROUND: The irritable bowel syndrome (IBS) has long been considered a functional disorder, but recent work has demonstrated clear biological signatures in immune, microbiome and enteric nervous systems of patients with IBS. Despite this new knowledge, there is still no clear biological marker of IBS, with patient symptom reporting and exclusion of organic disease the main criteria for diagnosis. We aimed to perform a systematic review and meta-analysis to identify consistent biomarkers for IBS in serum and stool samples.
METHODS: We searched Medline, EMBASE, Cochrane Library, Web of Science and Scopus to obtain all relevant publications published between 1992 and January 2026. Original, peer-reviewed research articles including adults with IBS and healthy or outpatient controls, and/or patients with organic gastrointestinal conditions (e.g. IBD) were included. All articles had quantification of blood and faecal markers between IBS and controls. Descriptive data presented as median and range or median (interquartile range) was converted to mean ± SD. To account for methodological assay differences between studies, standardised mean difference (SMD) with 95% confidence interval was used as the primary outcome measure for the meta-analyses, with a random effects model fitted to the data.
FINDINGS: The search strategy identified 55,444 citations across all databases. 124 studies were included encompassing 14,930 patients with IBS, 7544 healthy/asymptomatic controls and 4317 patients with organic diseases. The top serum discriminators between IBS and healthy controls were TNF-⍺ (13 studies, 1025 controls and 1244 IBS, SMD = 2.74, 95% CI = 0.70, 4.70, p = 0.006), IL-6 (13 studies, 736 controls and 1022 IBS, SMD = 1.87, 95% CI = 0.13, 3.61, p = 0.035) and IFN-ɣ (4 studies, n = 195 controls, n = 372 IBS, SMD = 2.79, 95% CI = 1.07, 4.51, p = 0.002). For faecal markers calprotectin was significantly higher in patients with IBS over controls (11 studies, 1624 controls and 1383 IBS, SMD = 0.75, 95% CI = 0.30, 1.21, p = 0.001), while faecal valerate levels were lower in IBS versus controls (4 studies, 290 controls and 488 IBS, SMD = -0.79, 95% CI = -1.48, -0.11, p = 0.02). For discriminating IBS overall from organic diseases, serum albumin (4 studies, 282 IBS and 312 organic, SMD = 2.15, 95% CI = 0.20, 4.11, p = 0.031) and faecal calprotectin (16 studies, 1591 IBS and 1685 organic, SMD = -1.13, 95% CI = -1.51, -0.75, p < 0.0001) were significantly different. In discriminating IBS subtypes from controls, only diarrhoeal IBS (IBS-D) could be distinguished by albumin (3 studies, 248 controls and 219 IBS-D, SMD = -0.39, 95% CI = -0.68, -0.11, p = 0.007) and IL-6 (4 studies, 153 IBS-D and 169 controls, SMD = 2.53, 95% CI = 0.86, 4.21, p = 0.003). Heterogeneity across the studies ranged from moderate to high, but few overly influential studies were identified between comparisons.
INTERPRETATION: Patients with IBS exhibit increased peripheral cytokine levels that are consistent with reports of increased epithelial permeability and may be important in distinguishing subgroups of IBS patients. Patients with IBS also demonstrated higher faecal calprotectin levels than healthy individuals, although these levels were still significantly lower than patients with organic diseases. Similarly, patients with IBS-D have lower serum albumin levels compared to healthy controls, while patients with organic disease had lower levels compared to patients with IBS, irrespective of subtype. There are clear biological signatures at play in IBS patients that may be useful clinically in establishing IBS diagnosis and may indicate the mechanisms of disease symptoms.
FUNDING: National Health and Medical Research Council Centre for Research Excellence in Digestive Health (NJT, SK) G180219.
Additional Links: PMID-41793943
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@article {pmid41793943,
year = {2026},
author = {Burns, GL and Roberts, F and Wark, JA and Fowler, S and Jones, MP and Duncanson, K and Talley, NJ and Keely, S},
title = {Serological and faecal markers of irritable bowel syndrome: a systematic review and meta-analysis.},
journal = {EBioMedicine},
volume = {126},
number = {},
pages = {106198},
doi = {10.1016/j.ebiom.2026.106198},
pmid = {41793943},
issn = {2352-3964},
abstract = {BACKGROUND: The irritable bowel syndrome (IBS) has long been considered a functional disorder, but recent work has demonstrated clear biological signatures in immune, microbiome and enteric nervous systems of patients with IBS. Despite this new knowledge, there is still no clear biological marker of IBS, with patient symptom reporting and exclusion of organic disease the main criteria for diagnosis. We aimed to perform a systematic review and meta-analysis to identify consistent biomarkers for IBS in serum and stool samples.
METHODS: We searched Medline, EMBASE, Cochrane Library, Web of Science and Scopus to obtain all relevant publications published between 1992 and January 2026. Original, peer-reviewed research articles including adults with IBS and healthy or outpatient controls, and/or patients with organic gastrointestinal conditions (e.g. IBD) were included. All articles had quantification of blood and faecal markers between IBS and controls. Descriptive data presented as median and range or median (interquartile range) was converted to mean ± SD. To account for methodological assay differences between studies, standardised mean difference (SMD) with 95% confidence interval was used as the primary outcome measure for the meta-analyses, with a random effects model fitted to the data.
FINDINGS: The search strategy identified 55,444 citations across all databases. 124 studies were included encompassing 14,930 patients with IBS, 7544 healthy/asymptomatic controls and 4317 patients with organic diseases. The top serum discriminators between IBS and healthy controls were TNF-⍺ (13 studies, 1025 controls and 1244 IBS, SMD = 2.74, 95% CI = 0.70, 4.70, p = 0.006), IL-6 (13 studies, 736 controls and 1022 IBS, SMD = 1.87, 95% CI = 0.13, 3.61, p = 0.035) and IFN-ɣ (4 studies, n = 195 controls, n = 372 IBS, SMD = 2.79, 95% CI = 1.07, 4.51, p = 0.002). For faecal markers calprotectin was significantly higher in patients with IBS over controls (11 studies, 1624 controls and 1383 IBS, SMD = 0.75, 95% CI = 0.30, 1.21, p = 0.001), while faecal valerate levels were lower in IBS versus controls (4 studies, 290 controls and 488 IBS, SMD = -0.79, 95% CI = -1.48, -0.11, p = 0.02). For discriminating IBS overall from organic diseases, serum albumin (4 studies, 282 IBS and 312 organic, SMD = 2.15, 95% CI = 0.20, 4.11, p = 0.031) and faecal calprotectin (16 studies, 1591 IBS and 1685 organic, SMD = -1.13, 95% CI = -1.51, -0.75, p < 0.0001) were significantly different. In discriminating IBS subtypes from controls, only diarrhoeal IBS (IBS-D) could be distinguished by albumin (3 studies, 248 controls and 219 IBS-D, SMD = -0.39, 95% CI = -0.68, -0.11, p = 0.007) and IL-6 (4 studies, 153 IBS-D and 169 controls, SMD = 2.53, 95% CI = 0.86, 4.21, p = 0.003). Heterogeneity across the studies ranged from moderate to high, but few overly influential studies were identified between comparisons.
INTERPRETATION: Patients with IBS exhibit increased peripheral cytokine levels that are consistent with reports of increased epithelial permeability and may be important in distinguishing subgroups of IBS patients. Patients with IBS also demonstrated higher faecal calprotectin levels than healthy individuals, although these levels were still significantly lower than patients with organic diseases. Similarly, patients with IBS-D have lower serum albumin levels compared to healthy controls, while patients with organic disease had lower levels compared to patients with IBS, irrespective of subtype. There are clear biological signatures at play in IBS patients that may be useful clinically in establishing IBS diagnosis and may indicate the mechanisms of disease symptoms.
FUNDING: National Health and Medical Research Council Centre for Research Excellence in Digestive Health (NJT, SK) G180219.},
}
RevDate: 2026-03-07
Indoor airborne bacterial communities and adult lung health: A cross-sectional study.
International journal of hygiene and environmental health, 274:114780 pii:S1438-4639(26)00040-4 [Epub ahead of print].
BACKGROUND AND OBJECTIVE: Indoor microbial exposures influence respiratory health, yet how men and women respond differently to airborne bacterial communities remains unclear. This study aimed to assess sex-specific associations between indoor airborne bacteria, and lung function, and airway inflammation in adults.
METHODS: Airborne dust was collected from the bedrooms of 1038 adults (463 men, 575 women) across five Nordic cities as part of the European Community Respiratory Health Survey (ECRHS) III. Bacterial communities were profiled using 16S rRNA amplicon sequencing. Bacterial and endotoxin loads were quantified via quantitative PCR (qPCR) and the Limulus amebocyte lysate (LAL) assay, respectively. Multivariable linear regression models stratified by sex were used to examine associations with lung function and airway inflammation.
RESULTS: Greater indoor bacterial diversity was associated with higher lung function in men (FEV1 β = 0.17, 95% CI: 0.05 to 0.29, P = 0.003) and higher FeNO levels in women (β = 2.44, 95% CI: 0.73 to 4.15, P = 0.005). Endotoxin load was positively associated with FeNO in women (β = 0.37, 95% CI: 0.05 to 0.70, P = 0.02), but not in men. Genera from Actinobacteriota and Bacilli were associated with higher lung function, while Clostridia was linked to lower lung function and reduced FeNO. In contrast, several genera from Actinobacteriota and Gammaproteobacteria were positively associated with FeNO.
CONCLUSIONS: Indoor bacterial exposures were associated with respiratory health in a sex-specific pattern. These findings highlight the importance of microbial composition in shaping adult lung health and underscore the need for sex-specific approaches in future epidemiological research.
Additional Links: PMID-41793899
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@article {pmid41793899,
year = {2026},
author = {Amin, H and Cramer, C and Finster, K and Real, FG and Gislason, T and Holm, M and Janson, C and Jögi, NO and Jogi, R and Malinovschi, A and Modig, L and Norbäck, D and Shigdel, R and Sigsgaard, T and Svanes, C and Thorarinsdottir, H and Wouters, IM and Šantl-Temkiv, T and Schlünssen, V and Bertelsen, RJ},
title = {Indoor airborne bacterial communities and adult lung health: A cross-sectional study.},
journal = {International journal of hygiene and environmental health},
volume = {274},
number = {},
pages = {114780},
doi = {10.1016/j.ijheh.2026.114780},
pmid = {41793899},
issn = {1618-131X},
abstract = {BACKGROUND AND OBJECTIVE: Indoor microbial exposures influence respiratory health, yet how men and women respond differently to airborne bacterial communities remains unclear. This study aimed to assess sex-specific associations between indoor airborne bacteria, and lung function, and airway inflammation in adults.
METHODS: Airborne dust was collected from the bedrooms of 1038 adults (463 men, 575 women) across five Nordic cities as part of the European Community Respiratory Health Survey (ECRHS) III. Bacterial communities were profiled using 16S rRNA amplicon sequencing. Bacterial and endotoxin loads were quantified via quantitative PCR (qPCR) and the Limulus amebocyte lysate (LAL) assay, respectively. Multivariable linear regression models stratified by sex were used to examine associations with lung function and airway inflammation.
RESULTS: Greater indoor bacterial diversity was associated with higher lung function in men (FEV1 β = 0.17, 95% CI: 0.05 to 0.29, P = 0.003) and higher FeNO levels in women (β = 2.44, 95% CI: 0.73 to 4.15, P = 0.005). Endotoxin load was positively associated with FeNO in women (β = 0.37, 95% CI: 0.05 to 0.70, P = 0.02), but not in men. Genera from Actinobacteriota and Bacilli were associated with higher lung function, while Clostridia was linked to lower lung function and reduced FeNO. In contrast, several genera from Actinobacteriota and Gammaproteobacteria were positively associated with FeNO.
CONCLUSIONS: Indoor bacterial exposures were associated with respiratory health in a sex-specific pattern. These findings highlight the importance of microbial composition in shaping adult lung health and underscore the need for sex-specific approaches in future epidemiological research.},
}
RevDate: 2026-03-07
Developing fast scan cyclic voltammetry at carbon fiber microelectrodes to quantify short chain fatty acids in situ.
Bioelectrochemistry (Amsterdam, Netherlands), 171:109266 pii:S1567-5394(26)00052-6 [Epub ahead of print].
Acetic, propionic, and butyric acids are short chain fatty acids (SCFAs) and the most abundant metabolites produced by gut bacteria. To uncover mechanistic insights of their function throughout the body, it is critical to measure rapid SCFA fluxes in sites of action such as brain, muscle, and skin. Current approaches have focused on fecal and plasma measurements, where SCFA levels are low and not representative of tissue-specific concentrations or fluxes. Thus, a rapid, in situ methodology is needed. Fast scan cyclic voltammetry (FSCV) at carbon fiber microelectrodes (CFMs) has the spatiotemporal resolution to fill this need. However, the electrochemical response of CFMs to SCFAs have not been explored until now. By coupling FSCV at CFMs with flow injection analysis of each SCFA, we demonstrate there are distinct peaks in the cyclic voltammograms for each fatty acid. Some of these peaks display faradaic behavior in scan rate, holding potential, and switching potential experiments. Interestingly, we identify several peaks that are concentration-sensitive and therefore are promising quantifiable markers of SCFA dynamics and fluxes. This work lays the foundation in understanding the response of CFMs to fatty acids and demonstrate the utility of FSCV at CFMs for the in situ quantitation of SCFAs.
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@article {pmid41793893,
year = {2026},
author = {Narla, T and Nudurupati, U and Ou, Y},
title = {Developing fast scan cyclic voltammetry at carbon fiber microelectrodes to quantify short chain fatty acids in situ.},
journal = {Bioelectrochemistry (Amsterdam, Netherlands)},
volume = {171},
number = {},
pages = {109266},
doi = {10.1016/j.bioelechem.2026.109266},
pmid = {41793893},
issn = {1878-562X},
abstract = {Acetic, propionic, and butyric acids are short chain fatty acids (SCFAs) and the most abundant metabolites produced by gut bacteria. To uncover mechanistic insights of their function throughout the body, it is critical to measure rapid SCFA fluxes in sites of action such as brain, muscle, and skin. Current approaches have focused on fecal and plasma measurements, where SCFA levels are low and not representative of tissue-specific concentrations or fluxes. Thus, a rapid, in situ methodology is needed. Fast scan cyclic voltammetry (FSCV) at carbon fiber microelectrodes (CFMs) has the spatiotemporal resolution to fill this need. However, the electrochemical response of CFMs to SCFAs have not been explored until now. By coupling FSCV at CFMs with flow injection analysis of each SCFA, we demonstrate there are distinct peaks in the cyclic voltammograms for each fatty acid. Some of these peaks display faradaic behavior in scan rate, holding potential, and switching potential experiments. Interestingly, we identify several peaks that are concentration-sensitive and therefore are promising quantifiable markers of SCFA dynamics and fluxes. This work lays the foundation in understanding the response of CFMs to fatty acids and demonstrate the utility of FSCV at CFMs for the in situ quantitation of SCFAs.},
}
RevDate: 2026-03-07
Ingestible active capsule for gastrointestinal microbiome sampling.
Biomedical microdevices, 28(1):.
UNLABELLED: Various gastrointestinal disorders have been linked to gut microbiome dysbiosis, as it plays a critical role in immune regulation, metabolism, nutrient digestion, and pathogen suppression. However, the microbiome’s spatial variability across gastrointestinal segments and its intra- and interindividual differences complicate its study and clinical interpretation. While fecal DNA analysis is commonly used, stool samples only capture an accumulated signal and miss the spatial dynamics of microbial populations. To address this, we propose a modular sampling capsule capable of wirelessly collecting liquid. The capsule consists of two main modules: (i) an actuator module integrating a polymer-based microfluidic system with meltable wax-based opening valve, screen-printed microheater, cellulose membrane-based closing valve, evacuated sampling chamber with dried sample preservative material, filter membrane (size exclusion 150 μm), and sample extraction channel; and (ii) a control electronic module with communication, localization, and power supply units. The actuator module was validated in vitro using a diluted stool simulant (330 mg/mL) and an uncleaned porcine intestine. The opening valve activated within 3.6 ± 0.5 s at 120 ± 10 mA and 0.8 V. The sample was then filtered and aspirated into the sampling chamber within 1–2 s, and the closing valve sealed the inlet completely within 10 min. We overcame design, material, and fabrication challenges to construct an actuator module that functions effectively in liquids with variable physicochemical conditions (pH, chemical composition, viscosity, and particle size). These results demonstrate the feasibility of a controlled, segment-specific intestinal sampling capsule, representing a step towards precise and accurate microbiome profiling.
GRAPHICAL ABSTRACT: [Image: see text]
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10544-026-00802-4.
Additional Links: PMID-41793548
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@article {pmid41793548,
year = {2026},
author = {Shahadha, MH and Voigt, A and Gruner, D and Marschner, U and Le Floch, M and Hampe, J and Brauer, F and Schostek, S and Luniak, M and Bock, K and Richter, A},
title = {Ingestible active capsule for gastrointestinal microbiome sampling.},
journal = {Biomedical microdevices},
volume = {28},
number = {1},
pages = {},
pmid = {41793548},
issn = {1572-8781},
abstract = {UNLABELLED: Various gastrointestinal disorders have been linked to gut microbiome dysbiosis, as it plays a critical role in immune regulation, metabolism, nutrient digestion, and pathogen suppression. However, the microbiome’s spatial variability across gastrointestinal segments and its intra- and interindividual differences complicate its study and clinical interpretation. While fecal DNA analysis is commonly used, stool samples only capture an accumulated signal and miss the spatial dynamics of microbial populations. To address this, we propose a modular sampling capsule capable of wirelessly collecting liquid. The capsule consists of two main modules: (i) an actuator module integrating a polymer-based microfluidic system with meltable wax-based opening valve, screen-printed microheater, cellulose membrane-based closing valve, evacuated sampling chamber with dried sample preservative material, filter membrane (size exclusion 150 μm), and sample extraction channel; and (ii) a control electronic module with communication, localization, and power supply units. The actuator module was validated in vitro using a diluted stool simulant (330 mg/mL) and an uncleaned porcine intestine. The opening valve activated within 3.6 ± 0.5 s at 120 ± 10 mA and 0.8 V. The sample was then filtered and aspirated into the sampling chamber within 1–2 s, and the closing valve sealed the inlet completely within 10 min. We overcame design, material, and fabrication challenges to construct an actuator module that functions effectively in liquids with variable physicochemical conditions (pH, chemical composition, viscosity, and particle size). These results demonstrate the feasibility of a controlled, segment-specific intestinal sampling capsule, representing a step towards precise and accurate microbiome profiling.
GRAPHICAL ABSTRACT: [Image: see text]
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10544-026-00802-4.},
}
RevDate: 2026-03-07
Subgingival Microbial Signatures Associated With Apical Periodontitis Identified by Next Generation Sequencing and Predictive Modelling.
International endodontic journal [Epub ahead of print].
AIMS: To assess the relationship between endodontic and subgingival bacterial communities in individuals with apical periodontitis (AP), and to identify disease-associated subgingival microbial signatures. We propose that subgingival microbial communities exhibit a dysbiotic profile, defined by distinct bacterial signatures, which may provide complementary biological insights into AP.
METHODS: In this cross-sectional study, DNA was extracted from paired endodontic and subgingival samples from mesiobuccal sites of first molars in patients with AP (n = 25 sample pairs), and from subgingival samples from the same sites in healthy individuals (n = 34). Microbiota was explored using 16S rRNA sequencing. Alpha and beta diversity metrics were calculated. Differentially abundant taxa were identified using LEfSe. Random forest models based on the bacterial counts observed in the subgingival samples were trained to classify the individuals with AP from the controls.
RESULTS: Within AP individuals, the subgingival communities differed from those present in root canals. Subgingival communities exhibited higher alpha diversity than root canal communities, irrespective of the clinical diagnosis (p < 0.001). Subgingival microbial communities in AP individuals exhibited a dysbiotic profile associated with enrichment of anaerobic and inflammophilic species (p < 0.05). Beta diversity analyses showed compositional differences between AP and control individuals, with Jaccard distance reaching statistical significance (p < 0.05), and Bray-Curtis indicating a borderline effect (p = 0.07). The best predictive model (Streptococcus sanguinis and Prevotella maculosa) achieved an accuracy of 89.8%, sensitivity of 80%, specificity of 97%, precision of 95.2%, and an AUC of 0.98.
CONCLUSIONS: Subgingival profiles from AP individuals are distinct from those in healthy controls, showing AP-associated dysbiosis. Specific subgingival bacterial signatures achieved high diagnostic accuracy, supporting the potential broader impact of AP on the subgingival microbiota.
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@article {pmid41793273,
year = {2026},
author = {Britos, M and Pellegrini, E and Hernández-Ríos, P and Garrido, M and Fernández, A and Tomás, I and León, R and Arredondo, A and Álvarez, G and Teuche, AH and Ríos, MH},
title = {Subgingival Microbial Signatures Associated With Apical Periodontitis Identified by Next Generation Sequencing and Predictive Modelling.},
journal = {International endodontic journal},
volume = {},
number = {},
pages = {},
doi = {10.1111/iej.70131},
pmid = {41793273},
issn = {1365-2591},
support = {1200098//FONDECYT/ ; 1251739//FONDECYT/ ; ID24I10282//Vice-Rectorate for Research and Development (VID), University of Chile/ ; //Chilean Government/ ; },
abstract = {AIMS: To assess the relationship between endodontic and subgingival bacterial communities in individuals with apical periodontitis (AP), and to identify disease-associated subgingival microbial signatures. We propose that subgingival microbial communities exhibit a dysbiotic profile, defined by distinct bacterial signatures, which may provide complementary biological insights into AP.
METHODS: In this cross-sectional study, DNA was extracted from paired endodontic and subgingival samples from mesiobuccal sites of first molars in patients with AP (n = 25 sample pairs), and from subgingival samples from the same sites in healthy individuals (n = 34). Microbiota was explored using 16S rRNA sequencing. Alpha and beta diversity metrics were calculated. Differentially abundant taxa were identified using LEfSe. Random forest models based on the bacterial counts observed in the subgingival samples were trained to classify the individuals with AP from the controls.
RESULTS: Within AP individuals, the subgingival communities differed from those present in root canals. Subgingival communities exhibited higher alpha diversity than root canal communities, irrespective of the clinical diagnosis (p < 0.001). Subgingival microbial communities in AP individuals exhibited a dysbiotic profile associated with enrichment of anaerobic and inflammophilic species (p < 0.05). Beta diversity analyses showed compositional differences between AP and control individuals, with Jaccard distance reaching statistical significance (p < 0.05), and Bray-Curtis indicating a borderline effect (p = 0.07). The best predictive model (Streptococcus sanguinis and Prevotella maculosa) achieved an accuracy of 89.8%, sensitivity of 80%, specificity of 97%, precision of 95.2%, and an AUC of 0.98.
CONCLUSIONS: Subgingival profiles from AP individuals are distinct from those in healthy controls, showing AP-associated dysbiosis. Specific subgingival bacterial signatures achieved high diagnostic accuracy, supporting the potential broader impact of AP on the subgingival microbiota.},
}
RevDate: 2026-03-07
CmpDate: 2026-03-07
Insights Into Highly Associated Co-Factors on HPV-Related Cervical Cancer.
Reviews in medical virology, 36(2):e70131.
Cervical cancer ranks among the most prevalent malignancies, representing a substantial threat to women's health. The incidence of cervical cancer is strongly correlated with persistent infections by high-risk human papillomavirus (HPV) types. Overall, the prevalence of HPV infection is high, with most cases being classified as recessive, latent, and subclinical. The predominant HPV types and overall infection rates exhibit variability across different tissue types, individuals, and regions. Numerous co-factors contribute to the processes underlying persistent HPV infection and carcinogenesis, including the microbiome, individual immune characteristics, and geographical population differences. Moreover, these factors affect the efficacy of chemotherapy and immunotherapy in cancer treatment. This review aims to summarise several key factors associated with HPV-related cervical cancer and discuss their mechanisms in promoting carcinogenesis in HPV-related malignancies. The insights gained may inform the development of more effective preventive and therapeutic strategies.
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@article {pmid41793176,
year = {2026},
author = {Zheng, L and Zhao, G and Zheng, L and Zou, Y and Zhang, S and Dong, J},
title = {Insights Into Highly Associated Co-Factors on HPV-Related Cervical Cancer.},
journal = {Reviews in medical virology},
volume = {36},
number = {2},
pages = {e70131},
doi = {10.1002/rmv.70131},
pmid = {41793176},
issn = {1099-1654},
mesh = {Humans ; *Uterine Cervical Neoplasms/virology/epidemiology/etiology ; Female ; *Papillomavirus Infections/complications/virology/epidemiology ; *Papillomaviridae/genetics/classification ; Prevalence ; Microbiota ; },
abstract = {Cervical cancer ranks among the most prevalent malignancies, representing a substantial threat to women's health. The incidence of cervical cancer is strongly correlated with persistent infections by high-risk human papillomavirus (HPV) types. Overall, the prevalence of HPV infection is high, with most cases being classified as recessive, latent, and subclinical. The predominant HPV types and overall infection rates exhibit variability across different tissue types, individuals, and regions. Numerous co-factors contribute to the processes underlying persistent HPV infection and carcinogenesis, including the microbiome, individual immune characteristics, and geographical population differences. Moreover, these factors affect the efficacy of chemotherapy and immunotherapy in cancer treatment. This review aims to summarise several key factors associated with HPV-related cervical cancer and discuss their mechanisms in promoting carcinogenesis in HPV-related malignancies. The insights gained may inform the development of more effective preventive and therapeutic strategies.},
}
MeSH Terms:
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Humans
*Uterine Cervical Neoplasms/virology/epidemiology/etiology
Female
*Papillomavirus Infections/complications/virology/epidemiology
*Papillomaviridae/genetics/classification
Prevalence
Microbiota
RevDate: 2026-03-09
CmpDate: 2026-03-07
Mechanistic Insights for Microbiome Application in Plant Disease Resistance.
Molecular plant pathology, 27(3):e70233.
Plant diseases caused by biotic and abiotic stresses pose a great threat to both plant health and yield. Plant microbiomes play a crucial role in improving disease resistance, representing a sustainable approach to enhance crop performance. Plant host factors, including genetic variation, metabolites and microRNA, shape the assembly and function of the plant microbiome, thereby augmenting disease resistance. This interplay presents opportunities for plant-mediated manipulation of microbiome to promote plant health. Multiple mechanisms are involved in the microbiome-mediated plant disease resistance, such as direct and indirect pathogen antagonism, niche pre-emption, alteration of microbiota and activation of plant defences. Nevertheless, the application of plant microbiome in the field remains limited due to the intrinsic complexity of plant-microbiome and environment-microbiome interactions. This review synthesises current knowledge on the roles of plant microbiomes in plant disease resistance. I further summarise the mechanisms underlying plant-guided microbiome modulation and probiotic-mediated disease suppression. I also raise work and challenges that should be addressed, with the ultimate goal of informing more efficient microbiome application in sustainable agriculture.
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@article {pmid41793016,
year = {2026},
author = {Yin, J},
title = {Mechanistic Insights for Microbiome Application in Plant Disease Resistance.},
journal = {Molecular plant pathology},
volume = {27},
number = {3},
pages = {e70233},
pmid = {41793016},
issn = {1364-3703},
support = {//Xinyang Normal University Scientific Research Start-up Fund./ ; 5250046//2025 Key Pilot Research Projects in Natural Sciences, Xinyang Normal University/ ; },
mesh = {*Microbiota/physiology ; *Disease Resistance/physiology ; *Plant Diseases/microbiology/immunology ; *Plants/microbiology ; },
abstract = {Plant diseases caused by biotic and abiotic stresses pose a great threat to both plant health and yield. Plant microbiomes play a crucial role in improving disease resistance, representing a sustainable approach to enhance crop performance. Plant host factors, including genetic variation, metabolites and microRNA, shape the assembly and function of the plant microbiome, thereby augmenting disease resistance. This interplay presents opportunities for plant-mediated manipulation of microbiome to promote plant health. Multiple mechanisms are involved in the microbiome-mediated plant disease resistance, such as direct and indirect pathogen antagonism, niche pre-emption, alteration of microbiota and activation of plant defences. Nevertheless, the application of plant microbiome in the field remains limited due to the intrinsic complexity of plant-microbiome and environment-microbiome interactions. This review synthesises current knowledge on the roles of plant microbiomes in plant disease resistance. I further summarise the mechanisms underlying plant-guided microbiome modulation and probiotic-mediated disease suppression. I also raise work and challenges that should be addressed, with the ultimate goal of informing more efficient microbiome application in sustainable agriculture.},
}
MeSH Terms:
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*Microbiota/physiology
*Disease Resistance/physiology
*Plant Diseases/microbiology/immunology
*Plants/microbiology
RevDate: 2026-03-07
Microbially Derived Essential Amino Acids Compensate for Dietary Deficiencies in an Ecologically Relevant Mammalian Host.
The ISME journal pii:8509917 [Epub ahead of print].
Protein is the main structural and functional component of cells, making it crucial for the survival of all living organisms. Yet mammalian herbivores and omnivores often consume diets deficient in the amount of protein required for growth, homeostasis, and reproduction. To compensate, mammals likely rely on their gut microbiota to synthesize essential amino acids (AAESS), particularly during periods of dietary protein limitation. We quantified the contribution of microbially synthesized AAESS to skeletal muscle in captive, wild-derived deer mice (Peromyscus maniculatus) fed diets varying in macromolecular quantity and quality. Using amino acid carbon isotope (δ13C) analysis combined with genetic sequencing, we assessed the origin of AAESS incorporated into host muscle and identified gut microbial taxa with the genetic potential for AAESS biosynthesis. We estimate that up to 25% of host muscle AAESS were microbially derived, with greater microbial contributions in mice fed diets containing low protein or more complex macronutrients. Gut microbial populations with the genetic potential for AAESS biosynthesis were more abundant in mice with larger contributions of microbially-derived AAESS in their tissues. These results demonstrate the crucial and likely pervasive role the gut microbiome plays in host protein metabolism, especially in mammals facing seasonal or persistent dietary protein limitation.
Additional Links: PMID-41792922
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PubMed:
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@article {pmid41792922,
year = {2026},
author = {Mertz, CM and Mancuso, CJ and Robinson, DM and Yeboah, LD and Fogel, ML and Takacs-Vesbach, C and Newsome, SD},
title = {Microbially Derived Essential Amino Acids Compensate for Dietary Deficiencies in an Ecologically Relevant Mammalian Host.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag044},
pmid = {41792922},
issn = {1751-7370},
abstract = {Protein is the main structural and functional component of cells, making it crucial for the survival of all living organisms. Yet mammalian herbivores and omnivores often consume diets deficient in the amount of protein required for growth, homeostasis, and reproduction. To compensate, mammals likely rely on their gut microbiota to synthesize essential amino acids (AAESS), particularly during periods of dietary protein limitation. We quantified the contribution of microbially synthesized AAESS to skeletal muscle in captive, wild-derived deer mice (Peromyscus maniculatus) fed diets varying in macromolecular quantity and quality. Using amino acid carbon isotope (δ13C) analysis combined with genetic sequencing, we assessed the origin of AAESS incorporated into host muscle and identified gut microbial taxa with the genetic potential for AAESS biosynthesis. We estimate that up to 25% of host muscle AAESS were microbially derived, with greater microbial contributions in mice fed diets containing low protein or more complex macronutrients. Gut microbial populations with the genetic potential for AAESS biosynthesis were more abundant in mice with larger contributions of microbially-derived AAESS in their tissues. These results demonstrate the crucial and likely pervasive role the gut microbiome plays in host protein metabolism, especially in mammals facing seasonal or persistent dietary protein limitation.},
}
RevDate: 2026-03-06
ENA1 deficiency attenuates Saccharomyces 'boulardii' probiotic yeast virulence in immunosuppressed mouse fungaemia model.
Communications biology pii:10.1038/s42003-026-09763-z [Epub ahead of print].
Recently, fungal infections originating from the probiotic Saccharomyces 'boulardii' yeast are increasingly reported. Here, we aimed to reveal the background of and to diminish the virulence of this yeast, mitigating infection risks in vulnerable patient groups. Product and human isolates of S. 'boulardii' were subjected to in-host selection and their subclone lineages were compared phenotypically to identify target phenotypes and associated genes. More virulent isolates showed signs of selection for high osmotic tolerance in immunosuppressed mouse model, hence the genes NHA1 and ENA1 were deleted in six different 'boulardii' backgrounds. Only ENA1 deletion diminished virulence in our mouse fungemia model and it retained the ability for gut colonization and its probiotic characteristics, including similar effects on the gut microbiome in gavaged mice. We also demonstrated the successful substitution of the ENA1 gene with an antilisterial bacteriocin, opening a strategy for safe strains with therapeutic effect. Our strain development approach highlighted the importance of testing various genetic backgrounds and resulted in engineered strains with drastically reduced capability to cause bloodstream infections even in immunosuppressed hosts, establishing the groundwork for safer probiotic yeast therapies in the future.
Additional Links: PMID-41792460
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PubMed:
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@article {pmid41792460,
year = {2026},
author = {Imre, A and Kovács, R and Jakab, Á and Harmath, A and Németh, B and Nagy, F and Forgács, L and Balázsi, D and Majoros, L and Benkő, Z and Crook, N and Pócsi, I and Pfliegler, WP},
title = {ENA1 deficiency attenuates Saccharomyces 'boulardii' probiotic yeast virulence in immunosuppressed mouse fungaemia model.},
journal = {Communications biology},
volume = {},
number = {},
pages = {},
doi = {10.1038/s42003-026-09763-z},
pmid = {41792460},
issn = {2399-3642},
abstract = {Recently, fungal infections originating from the probiotic Saccharomyces 'boulardii' yeast are increasingly reported. Here, we aimed to reveal the background of and to diminish the virulence of this yeast, mitigating infection risks in vulnerable patient groups. Product and human isolates of S. 'boulardii' were subjected to in-host selection and their subclone lineages were compared phenotypically to identify target phenotypes and associated genes. More virulent isolates showed signs of selection for high osmotic tolerance in immunosuppressed mouse model, hence the genes NHA1 and ENA1 were deleted in six different 'boulardii' backgrounds. Only ENA1 deletion diminished virulence in our mouse fungemia model and it retained the ability for gut colonization and its probiotic characteristics, including similar effects on the gut microbiome in gavaged mice. We also demonstrated the successful substitution of the ENA1 gene with an antilisterial bacteriocin, opening a strategy for safe strains with therapeutic effect. Our strain development approach highlighted the importance of testing various genetic backgrounds and resulted in engineered strains with drastically reduced capability to cause bloodstream infections even in immunosuppressed hosts, establishing the groundwork for safer probiotic yeast therapies in the future.},
}
RevDate: 2026-03-06
Preliminary insights into gut microbiome shifts as screening proxy for MASLD disease progression.
Scientific reports pii:10.1038/s41598-026-42368-4 [Epub ahead of print].
Additional Links: PMID-41792406
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PubMed:
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@article {pmid41792406,
year = {2026},
author = {Llirós Dupré, M and Buxó, M and Virolés, S and Pujolassos, M and Serra, I and Martínez, J and Lluansí, A and Bahí, A and Calle, M and Aldeguer, X},
title = {Preliminary insights into gut microbiome shifts as screening proxy for MASLD disease progression.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-42368-4},
pmid = {41792406},
issn = {2045-2322},
support = {2015 Research Initiation Grant #3//Societat Catalana de Digestologia/ ; Girona Townhall, 2017//Joan Bruguera Fund/ ; },
}
RevDate: 2026-03-06
Fecal microbiota transplantation in inflammatory bowel disease: a systematic review and meta-analysis of randomized controlled trials (2020-2025).
Inflammopharmacology [Epub ahead of print].
BACKGROUND: Fecal microbiota transplantation (FMT) has emerged as a therapeutic strategy for Inflammatory Bowel Disease (IBD) including ulcerative colitis (UC) and Crohn's disease (CD). Although multiple randomized controlled trials (RCTs) have been published in recent years, evidence remains fragmented regarding safety and efficacy. This systematic review and meta-analysis evaluated the efficacy and safety of microbiome-based interventions in Inflammatory Bowel Disease (IBD).
METHODS: A systematic search of PubMed, Cochrane CENTRAL and Embase was conducted for randomized controlled trials (RCTs) published between January 2020 and May 2025. Eligible studies compared donor FME with placebo, autologous FMT or standard therapy in adult patients with IBD. Primary outcomes were clinical remission and endoscopic improvement; secondary outcomes included maintenance of remission and adverse events. Risk of bias was assessed using the Cochrane RoB-2 tool. Meta-analyses were performed in R using the meta and meta for packages. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were estimated using common-effects and random-effects models.
RESULTS: Six RCTs involving 220-230 patients were included (majority UC patients, two trials CD). For induction of clinical remission, FMT was associated with significantly higher rates vs controls (OR = 3.24, 95% CI 1.43-7.41, p = 0.005) under a common-effect model; random-effects model showed similar point estimate but wide CI overlapping unity. Endoscopic response was strongly increased with FMT (OR = 6.80, 95% CI 2.96-15.63, p < 0.0001). Serious adverse events were more common in FMT arms but not statistically significant (common-effects OR ~ 2.05, 95% CI 0.72-5.81, p = 0.18). Evidence for maintenance of remission from two trials was limited and inconsistent.
CONCLUSION: Microbiome-based therapies, particularly FMT, significantly improved clinical and endoscopic remission in IBD (especially in UC) compared with control interventions, but safety signals and maintenance efficacy remain uncertain. Larger and strictly designed UC and CD-specific RCTs are needed to confirm long-term efficacy, clarify safety and define the role of microbiome-targeted therapies in IBD management.
Additional Links: PMID-41792366
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Citation:
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@article {pmid41792366,
year = {2026},
author = {Ikram, S and Ullah, M and Lee, J and Hasan, N and Yoo, JW and Khan, R and Naeem, M},
title = {Fecal microbiota transplantation in inflammatory bowel disease: a systematic review and meta-analysis of randomized controlled trials (2020-2025).},
journal = {Inflammopharmacology},
volume = {},
number = {},
pages = {},
pmid = {41792366},
issn = {1568-5608},
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) has emerged as a therapeutic strategy for Inflammatory Bowel Disease (IBD) including ulcerative colitis (UC) and Crohn's disease (CD). Although multiple randomized controlled trials (RCTs) have been published in recent years, evidence remains fragmented regarding safety and efficacy. This systematic review and meta-analysis evaluated the efficacy and safety of microbiome-based interventions in Inflammatory Bowel Disease (IBD).
METHODS: A systematic search of PubMed, Cochrane CENTRAL and Embase was conducted for randomized controlled trials (RCTs) published between January 2020 and May 2025. Eligible studies compared donor FME with placebo, autologous FMT or standard therapy in adult patients with IBD. Primary outcomes were clinical remission and endoscopic improvement; secondary outcomes included maintenance of remission and adverse events. Risk of bias was assessed using the Cochrane RoB-2 tool. Meta-analyses were performed in R using the meta and meta for packages. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were estimated using common-effects and random-effects models.
RESULTS: Six RCTs involving 220-230 patients were included (majority UC patients, two trials CD). For induction of clinical remission, FMT was associated with significantly higher rates vs controls (OR = 3.24, 95% CI 1.43-7.41, p = 0.005) under a common-effect model; random-effects model showed similar point estimate but wide CI overlapping unity. Endoscopic response was strongly increased with FMT (OR = 6.80, 95% CI 2.96-15.63, p < 0.0001). Serious adverse events were more common in FMT arms but not statistically significant (common-effects OR ~ 2.05, 95% CI 0.72-5.81, p = 0.18). Evidence for maintenance of remission from two trials was limited and inconsistent.
CONCLUSION: Microbiome-based therapies, particularly FMT, significantly improved clinical and endoscopic remission in IBD (especially in UC) compared with control interventions, but safety signals and maintenance efficacy remain uncertain. Larger and strictly designed UC and CD-specific RCTs are needed to confirm long-term efficacy, clarify safety and define the role of microbiome-targeted therapies in IBD management.},
}
RevDate: 2026-03-06
The microbiome of interstitial cystitis revealed by 2bRAD-M.
Scientific reports pii:10.1038/s41598-026-42249-w [Epub ahead of print].
Additional Links: PMID-41792350
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PubMed:
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@article {pmid41792350,
year = {2026},
author = {Gan, Y and Zhang, J and Yao, K and Jiang, R and Li, Z and Yang, Y},
title = {The microbiome of interstitial cystitis revealed by 2bRAD-M.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-42249-w},
pmid = {41792350},
issn = {2045-2322},
support = {82103239//National Natural Science Foundation of China/ ; 7244419//Beijing Municipal Natural Science Foundation/ ; },
}
RevDate: 2026-03-06
Spatial transcriptomics maps host-gut microbiome biogeography at high resolution.
Nature microbiology [Epub ahead of print].
Intermicrobial and host-microbial interactions are critical for the functioning of the gut microbiome, but few tools are available to measure these interactions in situ. Here we report a method for broad spatial sampling of microbiome-host interactions in the gut at high resolution (1 µm). This method combines enzymatic in situ polyadenylation of both bacterial and host RNA with spatial RNA sequencing to increase bacterial RNA recovery and enable transcriptomic analysis of low-abundance and spatially restricted microbial taxa. We benchmark the method against existing spatial transcriptomic workflows, demonstrating improved sensitivity and resolution. Application of this method in a mouse model of intestinal neoplasia revealed the biogeography of the mouse gut microbiome as function of location in the intestine, frequent strong intermicrobial interactions at short length scales and tumour-associated changes in the architecture of the host-microbiome interface. This method is compatible with widely available commercial platforms for spatial RNA sequencing and can therefore be readily adopted to study the role of short-range, bidirectional host-microbe interactions in microbiome health and disease.
Additional Links: PMID-41792309
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Citation:
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@article {pmid41792309,
year = {2026},
author = {Ntekas, I and Takayasu, L and McKellar, DW and Grodner, B and Holdener, C and Schweitzer, P and Park, YS and Sauthoff, M and Shi, Q and Brito, IL and De Vlaminck, I},
title = {Spatial transcriptomics maps host-gut microbiome biogeography at high resolution.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
pmid = {41792309},
issn = {2058-5276},
abstract = {Intermicrobial and host-microbial interactions are critical for the functioning of the gut microbiome, but few tools are available to measure these interactions in situ. Here we report a method for broad spatial sampling of microbiome-host interactions in the gut at high resolution (1 µm). This method combines enzymatic in situ polyadenylation of both bacterial and host RNA with spatial RNA sequencing to increase bacterial RNA recovery and enable transcriptomic analysis of low-abundance and spatially restricted microbial taxa. We benchmark the method against existing spatial transcriptomic workflows, demonstrating improved sensitivity and resolution. Application of this method in a mouse model of intestinal neoplasia revealed the biogeography of the mouse gut microbiome as function of location in the intestine, frequent strong intermicrobial interactions at short length scales and tumour-associated changes in the architecture of the host-microbiome interface. This method is compatible with widely available commercial platforms for spatial RNA sequencing and can therefore be readily adopted to study the role of short-range, bidirectional host-microbe interactions in microbiome health and disease.},
}
RevDate: 2026-03-06
HIV-associated gut microbiome influences gut mucosal immunity.
Nature reviews. Gastroenterology & hepatology [Epub ahead of print].
Additional Links: PMID-41792269
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Citation:
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@article {pmid41792269,
year = {2026},
author = {Ray, K},
title = {HIV-associated gut microbiome influences gut mucosal immunity.},
journal = {Nature reviews. Gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
pmid = {41792269},
issn = {1759-5053},
}
RevDate: 2026-03-06
Characterization of bacterial microbiome and molecular detection of rickettsiosis in free-living ticks (Amblyomma sculptum Berlese, 1888).
Scientific reports pii:10.1038/s41598-026-38069-7 [Epub ahead of print].
Amblyomma sculptum is a major tick species in southeastern Brazil and an important vector in the epidemiology of Brazilian Spotted Fever (BSF). This study characterized the bacterial microbiome of free-living A. sculptum ticks in a BSF-endemic area, focusing on differences among developmental stages and sexes, and investigated rickettsial agents using 16S rRNA gene (V3-V4) sequencing. A total of 154 ticks were collected and analysed as 13 pooled samples grouped by stage and sex. Sequencing identified a diverse bacterial community of 180 genera, dominated by Sphingomonas, Nocardioides, Actinomycetospora and Methylobacterium, alongside genera of potential zoonotic relevance such as Rickettsia, Anaplasma, Ehrlichia and Coxiella, mainly in nymph pools. Alpha and beta diversity analysis showed that microbial community composition differed among stages and sexes, with adult males exhibiting higher richness and compositional dispersion, whereas nymphs showed reduced diversity and tighter clustering. Because 16S sequencing does not allow species-level identification of rickettsiae, positive samples were further analysed by PCR amplification and sequencing of the gltA gene, which identified Rickettsia bellii. Together, these results highlight stage- and sex-associated patterns in the microbiome of free-living A. sculptum and support the use of integrated microbiome profiling and targeted rickettsial detection in ecological and epidemiological studies of tick-borne diseases.
Additional Links: PMID-41792267
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@article {pmid41792267,
year = {2026},
author = {Almeida, AP and Moncau-Gadbem, CT and Goes, CP and Garcia, IS and da Silva, TR and Clemente, LG and Coutinho, LL},
title = {Characterization of bacterial microbiome and molecular detection of rickettsiosis in free-living ticks (Amblyomma sculptum Berlese, 1888).},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-38069-7},
pmid = {41792267},
issn = {2045-2322},
abstract = {Amblyomma sculptum is a major tick species in southeastern Brazil and an important vector in the epidemiology of Brazilian Spotted Fever (BSF). This study characterized the bacterial microbiome of free-living A. sculptum ticks in a BSF-endemic area, focusing on differences among developmental stages and sexes, and investigated rickettsial agents using 16S rRNA gene (V3-V4) sequencing. A total of 154 ticks were collected and analysed as 13 pooled samples grouped by stage and sex. Sequencing identified a diverse bacterial community of 180 genera, dominated by Sphingomonas, Nocardioides, Actinomycetospora and Methylobacterium, alongside genera of potential zoonotic relevance such as Rickettsia, Anaplasma, Ehrlichia and Coxiella, mainly in nymph pools. Alpha and beta diversity analysis showed that microbial community composition differed among stages and sexes, with adult males exhibiting higher richness and compositional dispersion, whereas nymphs showed reduced diversity and tighter clustering. Because 16S sequencing does not allow species-level identification of rickettsiae, positive samples were further analysed by PCR amplification and sequencing of the gltA gene, which identified Rickettsia bellii. Together, these results highlight stage- and sex-associated patterns in the microbiome of free-living A. sculptum and support the use of integrated microbiome profiling and targeted rickettsial detection in ecological and epidemiological studies of tick-borne diseases.},
}
RevDate: 2026-03-06
Proline/serine-rich coiled-coil 1 alleviates atherosclerosis via remodeling tryptophan metabolism mediated by Akkermansia muciniphila.
Experimental & molecular medicine [Epub ahead of print].
Genome-wide association studies have implicated proline/serine-rich coiled-coil 1 (PSRC1) in coronary artery disease (CAD) pathogenesis. Our previous studies demonstrated that Psrc1 deficiency accelerates atherosclerosis via gut microbial dysbiosis, characterized by a substantial depletion of Akkermansia muciniphila. Recent studies implicate microbiome-dependent tryptophan metabolism as a novel checkpoint in atherosclerosis, with specific microbial taxa regulating metabolite-driven immune responses. The mechanism by which Psrc1 modulates atherosclerosis through A. muciniphila and its regulation of tryptophan metabolism remains unclear. Here Psrc1 knockout mice exhibited reduced colonic mucin content, altered tryptophan metabolic enzyme expression and diminished levels of Trp metabolites including indoleacetic acid (IAA), with concomitant suppression of Ahr signaling in macrophages. In vivo analysis revealed that Psrc1 knockout diminishes Ahr through A. muciniphila-dependent IAA depletion. In vitro experiments further uncovered that Psrc1 stabilizes Ahr protein via ubiquitin carboxyl terminal hydrolase L3 (Uchl3)-mediated deubiquitylation. In addition, we identified plasma IAA levels positively correlating with decreased PSRC1 expression in peripheral blood mononuclear cells from patients with CAD. Furthermore, therapeutic restoration of a live A. muciniphila-IAA axis through oral supplementation reversed atherosclerosis in Psrc1 knockout mice. Notably, oral IAA supplementation substantially ameliorated atherosclerosis in Psrc1 knockout mice by suppressing plaque macrophage apoptosis. Crucially, co-administration of the Ahr antagonist CH-223191 abolished these benefits, confirming Ahr dependence. Our findings position PSRC1 as a critical regulator of the A. muciniphila-IAA-Ahr axis and nominate microbiome-targeted Ahr activation as a precision therapeutic strategy for patients with CAD with PSRC1 loss-of-function variants.
Additional Links: PMID-41792233
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@article {pmid41792233,
year = {2026},
author = {Wu, Q and Hu, K and Wang, Q and Luo, T and Hu, L and Liu, J and Zou, D and Hu, J and Guo, Z},
title = {Proline/serine-rich coiled-coil 1 alleviates atherosclerosis via remodeling tryptophan metabolism mediated by Akkermansia muciniphila.},
journal = {Experimental & molecular medicine},
volume = {},
number = {},
pages = {},
pmid = {41792233},
issn = {2092-6413},
abstract = {Genome-wide association studies have implicated proline/serine-rich coiled-coil 1 (PSRC1) in coronary artery disease (CAD) pathogenesis. Our previous studies demonstrated that Psrc1 deficiency accelerates atherosclerosis via gut microbial dysbiosis, characterized by a substantial depletion of Akkermansia muciniphila. Recent studies implicate microbiome-dependent tryptophan metabolism as a novel checkpoint in atherosclerosis, with specific microbial taxa regulating metabolite-driven immune responses. The mechanism by which Psrc1 modulates atherosclerosis through A. muciniphila and its regulation of tryptophan metabolism remains unclear. Here Psrc1 knockout mice exhibited reduced colonic mucin content, altered tryptophan metabolic enzyme expression and diminished levels of Trp metabolites including indoleacetic acid (IAA), with concomitant suppression of Ahr signaling in macrophages. In vivo analysis revealed that Psrc1 knockout diminishes Ahr through A. muciniphila-dependent IAA depletion. In vitro experiments further uncovered that Psrc1 stabilizes Ahr protein via ubiquitin carboxyl terminal hydrolase L3 (Uchl3)-mediated deubiquitylation. In addition, we identified plasma IAA levels positively correlating with decreased PSRC1 expression in peripheral blood mononuclear cells from patients with CAD. Furthermore, therapeutic restoration of a live A. muciniphila-IAA axis through oral supplementation reversed atherosclerosis in Psrc1 knockout mice. Notably, oral IAA supplementation substantially ameliorated atherosclerosis in Psrc1 knockout mice by suppressing plaque macrophage apoptosis. Crucially, co-administration of the Ahr antagonist CH-223191 abolished these benefits, confirming Ahr dependence. Our findings position PSRC1 as a critical regulator of the A. muciniphila-IAA-Ahr axis and nominate microbiome-targeted Ahr activation as a precision therapeutic strategy for patients with CAD with PSRC1 loss-of-function variants.},
}
RevDate: 2026-03-06
Gut microbiome signatures in colorectal neoplasia: a cross-sectional study across neoplasia stages and subtypes.
Gut pii:gutjnl-2025-337478 [Epub ahead of print].
BACKGROUND: While colorectal cancer (CRC) has been linked to the gut microbiome, it remains unclear whether specific microbial signatures are detectable in precursor lesions such as adenomatous polyps, serrated lesions or sessile serrated lesions.
OBJECTIVE: To assess gut microbiome taxonomic and functional associations with colorectal neoplasia presence, severity (non-advanced, advanced and CRC) and subtype and evaluate predictive potential in high-risk neoplasia.
DESIGN: Analysed cross-sectional stool metagenomes (pre-colonoscopy) from 1762 participants (97% White British) undergoing colonoscopy in the multicentre COLO-COHORT study. Neoplasia was classified per British Society of Gastroenterology surveillance guidelines. Linear mixed-effects models and random forest classifiers assessed taxonomic and functional associations, adjusting for dietary, clinical and lifestyle covariates.
RESULTS: Gut microbiome composition differences between individuals with and without neoplasia were statistically significant but minimal (R[2]=0.0008, p=0.03). A small number of species, including Mediterraneibacter faecis and Pseudoruminococcus massiliensis, and microbial pathways, including amino acid biosynthesis and β-lactam resistance, were modestly linked to neoplasia, particularly early lesions (q value <0.05). Associations were generally weak and attenuated after covariate adjustment. Predictive models combining the microbiome with clinical/demographic features modestly improved high-risk neoplasia classification (area under the curve=0.64 vs 0.58 for clinical/demographic features alone).
CONCLUSION: This large prospective cross-sectional study found weak and inconsistent associations between the gut microbiome and premalignant colorectal neoplasia, with no robust microbial signatures. Findings suggest that previously reported microbial shifts may emerge later in disease progression, potentially as a consequence rather than a cause of CRC. Longitudinal, multiomic studies disentangling temporal and causal pathways between the gut microbiome and neoplasia are required.
Additional Links: PMID-41791848
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PubMed:
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@article {pmid41791848,
year = {2026},
author = {Louca, P and Manning, S and Hackney, E and Sharp, L and Hull, MA and Koo, S and Young, GR and Taylor, GS and Dunneram, Y and Mitra, S and Hampton, JS and Dobson, C and Neilson, LJ and Addison, C and El-Omar, EM and , and Stewart, CJ and Rees, CJ},
title = {Gut microbiome signatures in colorectal neoplasia: a cross-sectional study across neoplasia stages and subtypes.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2025-337478},
pmid = {41791848},
issn = {1468-3288},
abstract = {BACKGROUND: While colorectal cancer (CRC) has been linked to the gut microbiome, it remains unclear whether specific microbial signatures are detectable in precursor lesions such as adenomatous polyps, serrated lesions or sessile serrated lesions.
OBJECTIVE: To assess gut microbiome taxonomic and functional associations with colorectal neoplasia presence, severity (non-advanced, advanced and CRC) and subtype and evaluate predictive potential in high-risk neoplasia.
DESIGN: Analysed cross-sectional stool metagenomes (pre-colonoscopy) from 1762 participants (97% White British) undergoing colonoscopy in the multicentre COLO-COHORT study. Neoplasia was classified per British Society of Gastroenterology surveillance guidelines. Linear mixed-effects models and random forest classifiers assessed taxonomic and functional associations, adjusting for dietary, clinical and lifestyle covariates.
RESULTS: Gut microbiome composition differences between individuals with and without neoplasia were statistically significant but minimal (R[2]=0.0008, p=0.03). A small number of species, including Mediterraneibacter faecis and Pseudoruminococcus massiliensis, and microbial pathways, including amino acid biosynthesis and β-lactam resistance, were modestly linked to neoplasia, particularly early lesions (q value <0.05). Associations were generally weak and attenuated after covariate adjustment. Predictive models combining the microbiome with clinical/demographic features modestly improved high-risk neoplasia classification (area under the curve=0.64 vs 0.58 for clinical/demographic features alone).
CONCLUSION: This large prospective cross-sectional study found weak and inconsistent associations between the gut microbiome and premalignant colorectal neoplasia, with no robust microbial signatures. Findings suggest that previously reported microbial shifts may emerge later in disease progression, potentially as a consequence rather than a cause of CRC. Longitudinal, multiomic studies disentangling temporal and causal pathways between the gut microbiome and neoplasia are required.},
}
RevDate: 2026-03-07
CmpDate: 2026-03-07
Antibiotic-associated dysbiosis and bispecific antibody outcomes in multiple myeloma.
Journal for immunotherapy of cancer, 14(3): pii:jitc-2025-014224.
BACKGROUND: The gut microbiota plays a critical role in regulating immune homeostasis and modulating responses to cancer immunotherapies. However, the impact of antibiotic-induced dysbiosis in patients with multiple myeloma (MM) treated with bispecific antibodies (BsAbs) remains unexplored. This multicenter, international study investigated whether antibiotic exposure prior to BsAb initiation alters the gut microbiome and affects clinical outcomes in patients with relapsed or refractory MM.
METHODS: We retrospectively analyzed 237 adult patients with MM treated with CD3-engaging BsAbs across six academic institutions. Antibiotic exposure was defined as the administration of any broad-spectrum, non-prophylactic antibiotic within 30 days before BsAb initiation. Clinical outcomes included overall survival (OS), progression-free survival (PFS), and cumulative incidence of relapse, evaluated using Kaplan-Meier estimates, log-rank tests, and multivariable Cox and competing-risk regression models. Additionally, in a subset of 24 patients, peripheral blood samples were collected prior to BsAb infusion for immunophenotyping, cytokine profiling, and serum short-chain fatty acid (SCFA) quantification, while stool samples for 16S ribosomal RNA (rRNA) sequencing were collected in a subset of 19 patients.
RESULTS: Broad-spectrum antibiotic exposure prior to BsAb therapy was associated with significantly inferior 1-year OS (60% (95% CI 44% to 81%) vs 77% (95% CI 71% to 83%), p=0.004) and PFS (26% (95% CI 14% to 47%) vs 53% (95% CI 46% to 61%), p<0.001), and higher relapse incidence (68% (95% CI 48% to 82%) vs 43% (95% CI 36% to 50%), p=0.004). In multivariable analyses, antibiotic exposure remained independently associated with poorer OS, PFS, and higher relapse risk. These associations were also observed within the subgroup of patients treated with CD3/B-cell maturation antibody-targeted BsAbs (n=155). Immunoprofiling revealed lower CD4[+] T-cell counts (p=0.017) and reduced circulating cytokine levels among antibiotic-exposed patients. 16S rRNA sequencing demonstrated a marked depletion of SCFA-producing genera, including Roseburia and Eubacterium, accompanied by lower serum SCFA concentrations. Moreover, microbiota composition before BsAb treatment correlated with therapy response and treatment-related toxicity.
CONCLUSIONS: Antibiotic-induced dysbiosis prior to BsAb therapy is associated with impaired immune reconstitution and inferior clinical outcomes in MM. These findings underscore the importance of antibiotic stewardship and suggest that microbiota-preserving strategies could enhance the efficacy of BsAb therapy in MM.
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@article {pmid41791791,
year = {2026},
author = {Corona, M and García-Vicente, R and Saez-Marin, AJ and Ancos-Pintado, R and Rodríguez-Garcia, A and Arroyo, A and Blanco, A and Chari, A and Martin, T and Wolf, J and Rey-Bua, B and Mateos, MV and Kortüm, KM and Riedhammer, C and Tamariz-Amador, LE and Valencia, E and Rodríguez-Otero, P and San Miguel, J and Ibarra, G and Oriol, A and Cedena, MT and López-Muñoz, N and Alonso, R and Calbacho, M and Sanchez-Pina, JM and Linares, M and Martínez-López, J},
title = {Antibiotic-associated dysbiosis and bispecific antibody outcomes in multiple myeloma.},
journal = {Journal for immunotherapy of cancer},
volume = {14},
number = {3},
pages = {},
doi = {10.1136/jitc-2025-014224},
pmid = {41791791},
issn = {2051-1426},
mesh = {Humans ; *Multiple Myeloma/drug therapy/mortality/immunology ; Male ; Female ; *Dysbiosis/chemically induced ; *Antibodies, Bispecific/therapeutic use/pharmacology ; *Anti-Bacterial Agents/adverse effects ; Middle Aged ; Aged ; Retrospective Studies ; Gastrointestinal Microbiome/drug effects ; Adult ; Treatment Outcome ; },
abstract = {BACKGROUND: The gut microbiota plays a critical role in regulating immune homeostasis and modulating responses to cancer immunotherapies. However, the impact of antibiotic-induced dysbiosis in patients with multiple myeloma (MM) treated with bispecific antibodies (BsAbs) remains unexplored. This multicenter, international study investigated whether antibiotic exposure prior to BsAb initiation alters the gut microbiome and affects clinical outcomes in patients with relapsed or refractory MM.
METHODS: We retrospectively analyzed 237 adult patients with MM treated with CD3-engaging BsAbs across six academic institutions. Antibiotic exposure was defined as the administration of any broad-spectrum, non-prophylactic antibiotic within 30 days before BsAb initiation. Clinical outcomes included overall survival (OS), progression-free survival (PFS), and cumulative incidence of relapse, evaluated using Kaplan-Meier estimates, log-rank tests, and multivariable Cox and competing-risk regression models. Additionally, in a subset of 24 patients, peripheral blood samples were collected prior to BsAb infusion for immunophenotyping, cytokine profiling, and serum short-chain fatty acid (SCFA) quantification, while stool samples for 16S ribosomal RNA (rRNA) sequencing were collected in a subset of 19 patients.
RESULTS: Broad-spectrum antibiotic exposure prior to BsAb therapy was associated with significantly inferior 1-year OS (60% (95% CI 44% to 81%) vs 77% (95% CI 71% to 83%), p=0.004) and PFS (26% (95% CI 14% to 47%) vs 53% (95% CI 46% to 61%), p<0.001), and higher relapse incidence (68% (95% CI 48% to 82%) vs 43% (95% CI 36% to 50%), p=0.004). In multivariable analyses, antibiotic exposure remained independently associated with poorer OS, PFS, and higher relapse risk. These associations were also observed within the subgroup of patients treated with CD3/B-cell maturation antibody-targeted BsAbs (n=155). Immunoprofiling revealed lower CD4[+] T-cell counts (p=0.017) and reduced circulating cytokine levels among antibiotic-exposed patients. 16S rRNA sequencing demonstrated a marked depletion of SCFA-producing genera, including Roseburia and Eubacterium, accompanied by lower serum SCFA concentrations. Moreover, microbiota composition before BsAb treatment correlated with therapy response and treatment-related toxicity.
CONCLUSIONS: Antibiotic-induced dysbiosis prior to BsAb therapy is associated with impaired immune reconstitution and inferior clinical outcomes in MM. These findings underscore the importance of antibiotic stewardship and suggest that microbiota-preserving strategies could enhance the efficacy of BsAb therapy in MM.},
}
MeSH Terms:
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Humans
*Multiple Myeloma/drug therapy/mortality/immunology
Male
Female
*Dysbiosis/chemically induced
*Antibodies, Bispecific/therapeutic use/pharmacology
*Anti-Bacterial Agents/adverse effects
Middle Aged
Aged
Retrospective Studies
Gastrointestinal Microbiome/drug effects
Adult
Treatment Outcome
RevDate: 2026-03-07
CmpDate: 2026-03-07
Exploring the transformative potential of multi-trophic strategies to enhance coral restoration and mitigate disease.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 381(1945):.
Unprecedented coral reef degradation from climate change, local impacts and disease requires time-critical development of innovative, cost-effective and ecologically grounded restoration strategies. Conventional restoration strategies to recover coral reef ecosystems largely focus on coral propagation, often de-prioritizing the broader ecological interactions that underpin reef resilience. However, coral reefs are complex ecosystems where other reef-associated organisms have fundamental and connected roles in nutrient cycling, biofiltration, pathogen control and microbiome stewardship. Integrating these key functional groups into restoration efforts in both the production phase (co-cultivation) and ecological recovery phase (ecological reconstruction) is required to advance coral restoration efforts toward more holistic coral reef ecological restoration frameworks. Integrating multi-trophic strategies provides a multifunctional, nature-based solution to enhance coral survival, mitigate disease outbreaks and promote overall ecosystem health. Here, we discuss the benefits of such a multi-trophic approach, where filter feeders, suspension feeders, detritivores and grazers are incorporated into the processes of reef restoration efforts. By leveraging positive species interactions based on facilitation theory, a multi-trophic approach provides a tool that not only enhances microbiome stewardship and coral reef restoration success but also reinforces the long-term sustainability of reef ecosystems in a changing climate. This article is part of the theme issue 'Managing infectious marine diseases in wild populations'.
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@article {pmid41791749,
year = {2026},
author = {Ribeiro, B and Duarte, G and Thomas, T and Reeves, S and Suggett, DJ and Peixoto, RS},
title = {Exploring the transformative potential of multi-trophic strategies to enhance coral restoration and mitigate disease.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {381},
number = {1945},
pages = {},
doi = {10.1098/rstb.2024.0323},
pmid = {41791749},
issn = {1471-2970},
mesh = {Animals ; *Coral Reefs ; *Anthozoa/physiology/microbiology ; *Conservation of Natural Resources/methods ; Climate Change ; *Environmental Restoration and Remediation/methods ; *Food Chain ; Microbiota ; },
abstract = {Unprecedented coral reef degradation from climate change, local impacts and disease requires time-critical development of innovative, cost-effective and ecologically grounded restoration strategies. Conventional restoration strategies to recover coral reef ecosystems largely focus on coral propagation, often de-prioritizing the broader ecological interactions that underpin reef resilience. However, coral reefs are complex ecosystems where other reef-associated organisms have fundamental and connected roles in nutrient cycling, biofiltration, pathogen control and microbiome stewardship. Integrating these key functional groups into restoration efforts in both the production phase (co-cultivation) and ecological recovery phase (ecological reconstruction) is required to advance coral restoration efforts toward more holistic coral reef ecological restoration frameworks. Integrating multi-trophic strategies provides a multifunctional, nature-based solution to enhance coral survival, mitigate disease outbreaks and promote overall ecosystem health. Here, we discuss the benefits of such a multi-trophic approach, where filter feeders, suspension feeders, detritivores and grazers are incorporated into the processes of reef restoration efforts. By leveraging positive species interactions based on facilitation theory, a multi-trophic approach provides a tool that not only enhances microbiome stewardship and coral reef restoration success but also reinforces the long-term sustainability of reef ecosystems in a changing climate. This article is part of the theme issue 'Managing infectious marine diseases in wild populations'.},
}
MeSH Terms:
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Animals
*Coral Reefs
*Anthozoa/physiology/microbiology
*Conservation of Natural Resources/methods
Climate Change
*Environmental Restoration and Remediation/methods
*Food Chain
Microbiota
RevDate: 2026-03-08
Harnessing the gut-heart axis for cardiovascular drug innovation: microbiome, metabolites, and personalized treatment strategies.
Clinica chimica acta; international journal of clinical chemistry, 587:120941 pii:S0009-8981(26)00123-3 [Epub ahead of print].
Cardiovascular disease (CVD) remains the leading cause of mortality worldwide despite major advances in pharmacotherapy. Emerging evidence reveals a pivotal role for the gut-heart axis, wherein gut microbiota are and their metabolites influence CV physiology, pathology, and drug responsiveness. Dysbiosis in conditions such as hypertension, atherosclerosis, and heart failure has been associated with altered production of bioactive metabolites including trimethylamine N-oxide, short-chain fatty acids, bile acids, and tryptophan derivatives. These metabolites have been shown to modulate inflammation, endothelial function, lipid metabolism, and myocardial remodeling. This review synthesizes current knowledge on microbiome-drug interactions in CV pharmacology, including how gut bacteria may metabolize drugs (e.g., digoxin, aspirin, warfarin) and how CV agents can shape microbial communities. We further explore microbiome-targeted therapeutic strategies-probiotics, prebiotics, postbiotics, fecal microbiota transplantation, and small-molecule inhibitors of harmful metabolites-highlighting their mechanisms, preclinical evidence, and translational potential. Integrating microbiome profiling with multi-omics platforms and artificial intelligence may enable personalized treatment strategies that optimize CV outcomes. While the gut-heart axis presents an exciting frontier for drug innovation, challenges remain in establishing causality, addressing inter-individual microbiome variability, managing confounding factors such as diet and medication use, and meeting regulatory requirements. Harnessing this bidirectional relationship holds promise for transforming CV pharmacotherapy from a one-size-fits-all approach to precision medicine grounded in host-microbe interactions.
Additional Links: PMID-41791695
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@article {pmid41791695,
year = {2026},
author = {Chandra, QM and Clister, D and Halim, P and Dalimunthe, A and Ichwan, M and Sari, DK and Umaya, C and Aktary, N and Rani, A and Park, MN and Kim, B and Syahputra, RA},
title = {Harnessing the gut-heart axis for cardiovascular drug innovation: microbiome, metabolites, and personalized treatment strategies.},
journal = {Clinica chimica acta; international journal of clinical chemistry},
volume = {587},
number = {},
pages = {120941},
doi = {10.1016/j.cca.2026.120941},
pmid = {41791695},
issn = {1873-3492},
abstract = {Cardiovascular disease (CVD) remains the leading cause of mortality worldwide despite major advances in pharmacotherapy. Emerging evidence reveals a pivotal role for the gut-heart axis, wherein gut microbiota are and their metabolites influence CV physiology, pathology, and drug responsiveness. Dysbiosis in conditions such as hypertension, atherosclerosis, and heart failure has been associated with altered production of bioactive metabolites including trimethylamine N-oxide, short-chain fatty acids, bile acids, and tryptophan derivatives. These metabolites have been shown to modulate inflammation, endothelial function, lipid metabolism, and myocardial remodeling. This review synthesizes current knowledge on microbiome-drug interactions in CV pharmacology, including how gut bacteria may metabolize drugs (e.g., digoxin, aspirin, warfarin) and how CV agents can shape microbial communities. We further explore microbiome-targeted therapeutic strategies-probiotics, prebiotics, postbiotics, fecal microbiota transplantation, and small-molecule inhibitors of harmful metabolites-highlighting their mechanisms, preclinical evidence, and translational potential. Integrating microbiome profiling with multi-omics platforms and artificial intelligence may enable personalized treatment strategies that optimize CV outcomes. While the gut-heart axis presents an exciting frontier for drug innovation, challenges remain in establishing causality, addressing inter-individual microbiome variability, managing confounding factors such as diet and medication use, and meeting regulatory requirements. Harnessing this bidirectional relationship holds promise for transforming CV pharmacotherapy from a one-size-fits-all approach to precision medicine grounded in host-microbe interactions.},
}
RevDate: 2026-03-06
Microbial communities and wing variation associated with ectoparasitic mites in medically important Mansonia mosquitoes (Diptera: Culicidae) from coconut plantation habitats in central Thailand.
Acta tropica pii:S0001-706X(26)00076-8 [Epub ahead of print].
This study presents the comprehensive assessment of the bacterial microbiome and the effects of ectoparasitic mites on wing morphometry in Mansonia mosquitoes, namely, Ma. annulifera, Ma. indiana, and Ma. uniformis from coconut-growing areas in central Thailand. High-throughput sequencing of the 16S ribosomal RNA gene (V3-V4 regions) generated 1,813,140 raw reads. Following quality control with the DADA2 pipeline, including filtering, denoising, merging, and chimera removal, 681,766 non-chimeric sequences were retained across nine libraries, yielding 467 unique amplicon sequence variants (ASVs). Distinct, species-specific bacterial community profiles were identified: Fructobacillus fructosus dominated Ma. annulifera (28.85% relative abundance), whereas Wolbachia was predominant in Ma. indiana (57.94%) and Ma. uniformis (80.87%). Although alpha diversity showed no significant interspecific differences (p > 0.05), beta-diversity analyses revealed clear species-specific clustering. Differential abundance testing further identified Rosenbergiella sp. as a biomarker for Ma. annulifera and Wolbachia sp. as highly enriched in Ma. indiana and Ma. uniformis. Geometric morphometric analysis revealed significant differences in mean centroid size among all mite infestation groups in Ma. annulifera (p < 0.05), but not in Ma. indiana or Ma. uniformis (p > 0.05). Shape analysis indicated that Ma. annulifera differed significantly only between the no-mite and high-intensity groups, Ma. indiana across all pairwise comparisons, and Ma. uniformis between the no-mite and high-intensity groups and between the low- and high-intensity groups (p < 0.05). This study provides new insights into Mansonia microbiome diversity and mite-associated morphological variation, with implications for mosquito ecology and disease transmission.
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@article {pmid41791635,
year = {2026},
author = {Laojun, S and Changbunjong, T and Bunchu, N and Chaiphongpachara, T},
title = {Microbial communities and wing variation associated with ectoparasitic mites in medically important Mansonia mosquitoes (Diptera: Culicidae) from coconut plantation habitats in central Thailand.},
journal = {Acta tropica},
volume = {},
number = {},
pages = {108042},
doi = {10.1016/j.actatropica.2026.108042},
pmid = {41791635},
issn = {1873-6254},
abstract = {This study presents the comprehensive assessment of the bacterial microbiome and the effects of ectoparasitic mites on wing morphometry in Mansonia mosquitoes, namely, Ma. annulifera, Ma. indiana, and Ma. uniformis from coconut-growing areas in central Thailand. High-throughput sequencing of the 16S ribosomal RNA gene (V3-V4 regions) generated 1,813,140 raw reads. Following quality control with the DADA2 pipeline, including filtering, denoising, merging, and chimera removal, 681,766 non-chimeric sequences were retained across nine libraries, yielding 467 unique amplicon sequence variants (ASVs). Distinct, species-specific bacterial community profiles were identified: Fructobacillus fructosus dominated Ma. annulifera (28.85% relative abundance), whereas Wolbachia was predominant in Ma. indiana (57.94%) and Ma. uniformis (80.87%). Although alpha diversity showed no significant interspecific differences (p > 0.05), beta-diversity analyses revealed clear species-specific clustering. Differential abundance testing further identified Rosenbergiella sp. as a biomarker for Ma. annulifera and Wolbachia sp. as highly enriched in Ma. indiana and Ma. uniformis. Geometric morphometric analysis revealed significant differences in mean centroid size among all mite infestation groups in Ma. annulifera (p < 0.05), but not in Ma. indiana or Ma. uniformis (p > 0.05). Shape analysis indicated that Ma. annulifera differed significantly only between the no-mite and high-intensity groups, Ma. indiana across all pairwise comparisons, and Ma. uniformis between the no-mite and high-intensity groups and between the low- and high-intensity groups (p < 0.05). This study provides new insights into Mansonia microbiome diversity and mite-associated morphological variation, with implications for mosquito ecology and disease transmission.},
}
RevDate: 2026-03-06
Genetically engineered eye-colonizing microbes that deliver the anti-inflammatory cytokine interleukin-10 enhance corneal tissue repair.
Cell reports pii:S2211-1247(26)00142-7 [Epub ahead of print].
Barrier surfaces harbor tissue-colonizing microbes that can shape local physiology and immunity. During corneal injury, inflammation can delay healing, resulting in loss of visual acuity. Standards of care include topical applications of therapies, which are quickly washed away, requiring a laborious treatment regimen to maintain efficacy. To address this problem, we engineered an eye-colonizing microbe, Corynebacterium mastitidis, to act as a long-term therapeutic delivery vehicle by secreting bioactive interleukin (IL)-10 using a native secretion signal that we identified using transposon mutagenesis. Engineered microbes stably colonize the eye and release mouse (mIL-10) or human IL-10 (hIL-10) that modulates local immunity and accelerates wound repair after an initial inoculation event. Further, hIL-10 producing C. mast can regulate inflammatory cytokine production in immune cells, highlighting the immune-regulatory capabilities of this live biotherapeutic product. These findings demonstrate that genetically engineered eye-colonizing bacteria can serve as a self-sustaining therapeutic platform to control inflammation and promote tissue repair.
Additional Links: PMID-41791375
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@article {pmid41791375,
year = {2026},
author = {Shane, J and Evans, M and Rigas, Y and Shanks, RMQ and St Leger, AJ},
title = {Genetically engineered eye-colonizing microbes that deliver the anti-inflammatory cytokine interleukin-10 enhance corneal tissue repair.},
journal = {Cell reports},
volume = {},
number = {},
pages = {117064},
doi = {10.1016/j.celrep.2026.117064},
pmid = {41791375},
issn = {2211-1247},
abstract = {Barrier surfaces harbor tissue-colonizing microbes that can shape local physiology and immunity. During corneal injury, inflammation can delay healing, resulting in loss of visual acuity. Standards of care include topical applications of therapies, which are quickly washed away, requiring a laborious treatment regimen to maintain efficacy. To address this problem, we engineered an eye-colonizing microbe, Corynebacterium mastitidis, to act as a long-term therapeutic delivery vehicle by secreting bioactive interleukin (IL)-10 using a native secretion signal that we identified using transposon mutagenesis. Engineered microbes stably colonize the eye and release mouse (mIL-10) or human IL-10 (hIL-10) that modulates local immunity and accelerates wound repair after an initial inoculation event. Further, hIL-10 producing C. mast can regulate inflammatory cytokine production in immune cells, highlighting the immune-regulatory capabilities of this live biotherapeutic product. These findings demonstrate that genetically engineered eye-colonizing bacteria can serve as a self-sustaining therapeutic platform to control inflammation and promote tissue repair.},
}
RevDate: 2026-03-06
From conventional to adapted microbiomes: Promoting high short-chain fatty acid yields and productivities from agricultural waste.
Journal of environmental management, 403:129216 pii:S0301-4797(26)00676-6 [Epub ahead of print].
Microbial consortia play an essential role in anaerobic fermentation (AF) devoted to the production of short-chain fatty acids (SCFAs) from organic wastes. AF is usually performed by a conventional anaerobic microbiome (CM) sourced from anaerobic digestion reactors. During AF, the microbiome undergoes an adaptation period to the imposed operational conditions and substrate characteristics, leading to the bio-enrichment of certain microorganisms. This work compared the use of CM and a bio-enriched microbiome (BM) as inoculum for AF of agricultural wastes in continuous stirred tank reactors (CSTR) with hydraulic retention time (HRT) of 8 d. The novelty of this study lies in demonstrating that using a BM enhances the production rate of SCFAs when compared to CM. BM, composed of adapted microorganisms previously working at an HRT of 10 d, allowed the highest SCFAs productivity (1.97 g/L·d) and concentration (15.6 g/L). Bioconversion efficiencies achieved with BM and CM (60.1 % and 71.8 %, respectively) were among the highest reported in literature. Microbiome analysis revealed inoculum-driven changes in the microbial community. However, Clostridium and Megasphaera, which are involved in the hydrolysis and acidification steps of AF and are associated with acetic acid formation and chain elongation, predominated in all cases (up to 48 % of the microbial abundance within the total community). These results evidenced the feasibility of operating CSTRs at an HRT of 8 d with diverse inoculum sources to maintain exceptionally high SCFA productivity and bioconversion. The outcomes also highlighted the robustness of the microbial community, even under short HRT, providing a novel strategy for AF processes optimization.
Additional Links: PMID-41791329
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@article {pmid41791329,
year = {2026},
author = {de Vicente, M and Tomás-Pejó, E and González-Fernández, C},
title = {From conventional to adapted microbiomes: Promoting high short-chain fatty acid yields and productivities from agricultural waste.},
journal = {Journal of environmental management},
volume = {403},
number = {},
pages = {129216},
doi = {10.1016/j.jenvman.2026.129216},
pmid = {41791329},
issn = {1095-8630},
abstract = {Microbial consortia play an essential role in anaerobic fermentation (AF) devoted to the production of short-chain fatty acids (SCFAs) from organic wastes. AF is usually performed by a conventional anaerobic microbiome (CM) sourced from anaerobic digestion reactors. During AF, the microbiome undergoes an adaptation period to the imposed operational conditions and substrate characteristics, leading to the bio-enrichment of certain microorganisms. This work compared the use of CM and a bio-enriched microbiome (BM) as inoculum for AF of agricultural wastes in continuous stirred tank reactors (CSTR) with hydraulic retention time (HRT) of 8 d. The novelty of this study lies in demonstrating that using a BM enhances the production rate of SCFAs when compared to CM. BM, composed of adapted microorganisms previously working at an HRT of 10 d, allowed the highest SCFAs productivity (1.97 g/L·d) and concentration (15.6 g/L). Bioconversion efficiencies achieved with BM and CM (60.1 % and 71.8 %, respectively) were among the highest reported in literature. Microbiome analysis revealed inoculum-driven changes in the microbial community. However, Clostridium and Megasphaera, which are involved in the hydrolysis and acidification steps of AF and are associated with acetic acid formation and chain elongation, predominated in all cases (up to 48 % of the microbial abundance within the total community). These results evidenced the feasibility of operating CSTRs at an HRT of 8 d with diverse inoculum sources to maintain exceptionally high SCFA productivity and bioconversion. The outcomes also highlighted the robustness of the microbial community, even under short HRT, providing a novel strategy for AF processes optimization.},
}
RevDate: 2026-03-06
Marine heatwaves alter shell microbiomes and denitrification capacity: An oyster family-specific response.
Marine pollution bulletin, 227:119503 pii:S0025-326X(26)00290-0 [Epub ahead of print].
Marine heatwaves (MHWs) are increasing in frequency and intensity, significantly affecting biodiversity and ecosystem processes. However, the impact of MHWs on microbiome structure and function, and whether such changes are influenced by intraspecific differences among hosts, remains unclear. This study investigated the effect of a simulated MHW on external shell microbiomes (alpha diversity, community and taxonomic compositions, and denitrification capacity) of four oyster families (1, 11, 14 and 15), with different levels of disease resistance and growth rate. Oysters were exposed to 29 °C (MHW) and 24 °C (control) temperatures for 6 days, followed by a 21-day recovery period. The MHW shifted bacterial community composition and decreased alpha diversity in Family 14, together with reductions in the relative abundance of Pseudomonadota and Planctomycetota, and in denitrification genes (nirK and nosZ). In Family 15, MHW exposure decreased the abundance of Rhizobiaceae and the denitrification gene nirS, which recovered within three weeks. Reduction in denitrification genes suggests a potential decline in nitrogen removal capacity, which could negatively affect coastal systems, as bioavailable nitrogen may accumulate and lead to eutrophication. Conversely, in Families 1 and 11 the shell microbiomes remained stable under heat stress. Although mechanisms were not directly assessed, these faster-growing families may possess physiological traits (e.g. efficient metabolism and filtration) that support the resilience of nitrogen-cycling microbes during thermal stress. This study highlights the importance of intraspecific differences among hosts in shaping microbiome responses to MHWs, suggesting that selecting certain oyster families could help maintain key microbial-driven processes like denitrification under climate stress.
Additional Links: PMID-41791313
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@article {pmid41791313,
year = {2026},
author = {Filippini, G and Bugnot, AB and O'Connor, W and Gribben, PE and Varkey, DR and Paulsen, IT and Dafforn, KA},
title = {Marine heatwaves alter shell microbiomes and denitrification capacity: An oyster family-specific response.},
journal = {Marine pollution bulletin},
volume = {227},
number = {},
pages = {119503},
doi = {10.1016/j.marpolbul.2026.119503},
pmid = {41791313},
issn = {1879-3363},
abstract = {Marine heatwaves (MHWs) are increasing in frequency and intensity, significantly affecting biodiversity and ecosystem processes. However, the impact of MHWs on microbiome structure and function, and whether such changes are influenced by intraspecific differences among hosts, remains unclear. This study investigated the effect of a simulated MHW on external shell microbiomes (alpha diversity, community and taxonomic compositions, and denitrification capacity) of four oyster families (1, 11, 14 and 15), with different levels of disease resistance and growth rate. Oysters were exposed to 29 °C (MHW) and 24 °C (control) temperatures for 6 days, followed by a 21-day recovery period. The MHW shifted bacterial community composition and decreased alpha diversity in Family 14, together with reductions in the relative abundance of Pseudomonadota and Planctomycetota, and in denitrification genes (nirK and nosZ). In Family 15, MHW exposure decreased the abundance of Rhizobiaceae and the denitrification gene nirS, which recovered within three weeks. Reduction in denitrification genes suggests a potential decline in nitrogen removal capacity, which could negatively affect coastal systems, as bioavailable nitrogen may accumulate and lead to eutrophication. Conversely, in Families 1 and 11 the shell microbiomes remained stable under heat stress. Although mechanisms were not directly assessed, these faster-growing families may possess physiological traits (e.g. efficient metabolism and filtration) that support the resilience of nitrogen-cycling microbes during thermal stress. This study highlights the importance of intraspecific differences among hosts in shaping microbiome responses to MHWs, suggesting that selecting certain oyster families could help maintain key microbial-driven processes like denitrification under climate stress.},
}
RevDate: 2026-03-08
CmpDate: 2026-03-08
The microbiome and PTSD: a scoping review across preclinical and clinical studies.
European journal of psychotraumatology, 17(1):2627060.
BACKGROUND: Posttraumatic Stress Disorder (PTSD) is a psychiatric condition that substantially impairs quality of life and global health. Emerging evidence implicates that the human microbiome contributes to PTSD pathophysiology via gut-brain-immune interactions, although the underlying mechanisms and therapeutic implications remain unclear.
OBJECTIVE: This review aimed to systematically map the evidence linking microbiome alterations to PTSD, with a focus on mechanistic pathways, therapeutic potential, and research gaps.
METHODS: This scoping review was conducted in Medline, Embase, and PsychINFO from inception to 18-03-2025. Eligible studies included human participants with PTSD and preclinical rodent models employing validated PTSD paradigms. Outcomes of interest included microbiome diversity and composition, gut-brain axis biomarkers, and effects of microbiome-targeted interventions.
RESULTS: Fifty studies were included, comprising 20 human, 29 preclinical and one cross-species study. Human observational studies frequently observed reduced overall microbial diversity, along with a loss of short-chain fatty acid (SCFA)-producing bacteria, such as Ruminococcaceae and Lachnospiraceae, and an increased abundance of Veillonella, Odoribacter, and Catenibacterium linked to gut permeability and inflammation. Human intervention studies testing probiotics, prebiotics, fermented soy, and dietary fibre showed preliminary evidence for symptom and related metabolic and inflammatory marker improvements; however, microbiome effects were inconsistent. Preclinical models revealed stress-induced reductions in Bifidobacteria, Verrucomicrobia, and Parabacteroides, and increases in Coprobacillus and Anaeroplasma. Functional consequences included impaired barrier integrity, altered SCFA levels, and heightened immune activation. Preclinical interventions, particularly Mycobacterium vaccae, as well as probiotics, synbiotics, acetate, and MDMA, mitigated microbial alterations, reduced anxiety-like behaviours, and modulated neuroimmune pathways.
CONCLUSION: Current evidence supports an association between PTSD and microbiome alterations, with convergent human and preclinical findings. However, human research remains limited by small, cross-sectional designs, which preclude causal inferences. Rigorous longitudinal and interventional studies are required to establish causality and assess microbiome-targeted therapies as adjuncts in PTSD treatment.
Additional Links: PMID-41790992
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@article {pmid41790992,
year = {2026},
author = {Berendse, R and Verkleij, M and Daams, J and Hemmings, S and Lindauer, R and Korosi, A and Zantvoord, JB and Lok, A},
title = {The microbiome and PTSD: a scoping review across preclinical and clinical studies.},
journal = {European journal of psychotraumatology},
volume = {17},
number = {1},
pages = {2627060},
doi = {10.1080/20008066.2026.2627060},
pmid = {41790992},
issn = {2000-8066},
mesh = {Humans ; Animals ; *Gastrointestinal Microbiome/physiology ; *Stress Disorders, Post-Traumatic/microbiology/physiopathology ; Disease Models, Animal ; },
abstract = {BACKGROUND: Posttraumatic Stress Disorder (PTSD) is a psychiatric condition that substantially impairs quality of life and global health. Emerging evidence implicates that the human microbiome contributes to PTSD pathophysiology via gut-brain-immune interactions, although the underlying mechanisms and therapeutic implications remain unclear.
OBJECTIVE: This review aimed to systematically map the evidence linking microbiome alterations to PTSD, with a focus on mechanistic pathways, therapeutic potential, and research gaps.
METHODS: This scoping review was conducted in Medline, Embase, and PsychINFO from inception to 18-03-2025. Eligible studies included human participants with PTSD and preclinical rodent models employing validated PTSD paradigms. Outcomes of interest included microbiome diversity and composition, gut-brain axis biomarkers, and effects of microbiome-targeted interventions.
RESULTS: Fifty studies were included, comprising 20 human, 29 preclinical and one cross-species study. Human observational studies frequently observed reduced overall microbial diversity, along with a loss of short-chain fatty acid (SCFA)-producing bacteria, such as Ruminococcaceae and Lachnospiraceae, and an increased abundance of Veillonella, Odoribacter, and Catenibacterium linked to gut permeability and inflammation. Human intervention studies testing probiotics, prebiotics, fermented soy, and dietary fibre showed preliminary evidence for symptom and related metabolic and inflammatory marker improvements; however, microbiome effects were inconsistent. Preclinical models revealed stress-induced reductions in Bifidobacteria, Verrucomicrobia, and Parabacteroides, and increases in Coprobacillus and Anaeroplasma. Functional consequences included impaired barrier integrity, altered SCFA levels, and heightened immune activation. Preclinical interventions, particularly Mycobacterium vaccae, as well as probiotics, synbiotics, acetate, and MDMA, mitigated microbial alterations, reduced anxiety-like behaviours, and modulated neuroimmune pathways.
CONCLUSION: Current evidence supports an association between PTSD and microbiome alterations, with convergent human and preclinical findings. However, human research remains limited by small, cross-sectional designs, which preclude causal inferences. Rigorous longitudinal and interventional studies are required to establish causality and assess microbiome-targeted therapies as adjuncts in PTSD treatment.},
}
MeSH Terms:
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Humans
Animals
*Gastrointestinal Microbiome/physiology
*Stress Disorders, Post-Traumatic/microbiology/physiopathology
Disease Models, Animal
RevDate: 2026-03-09
CmpDate: 2026-03-07
Association between oral microbiota and inflammatory bowel disease: A 2-sample Mendelian randomization study in East Asian populations.
Medicine, 105(10):e47909.
Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is increasingly prevalent in East Asia. Its pathogenesis is linked to microbiota dysbiosis via the oral-gut axis, but population-specific causal evidence remains scarce. This study aimed to clarify the causal associations between oral microbiota and UC/CD in East Asian populations using Mendelian randomization (MR), providing evidence for IBD etiology and precise prevention/treatment. A 2-sample MR approach was adopted, using genome-wide association study data of East Asian populations. Single nucleotide polymorphisms associated with tongue dorsum and salivary microbiota were selected as instrumental variables after rigorous screening (F-statistic > 10, linkage disequilibrium R2 = 0.001). Inverse variance weighted was the primary analysis method, supplemented by sensitivity tests (MR-PRESSO, MR-Egger intercept test, etc) and Benjamini-Hochberg multiple testing correction (false discovery rate < 0.05). A total of 82 oral microbiota taxa (22 families, 35 genera) were significantly causally associated with UC (FDR < 0.05), and 21 taxa (10 families, 12 genera) with CD (FDR < 0.05). High-risk taxa included Aggregatibacter and Streptococcus (OR > 1), while protective taxa included Fusobacterium_periodonticum_C_mgs_3022 and TM7x_unclassified_mgs_1084 (OR < 1). A distinct "mixed effect" was identified: the Streptococcus genus was risky for UC but protective for CD; genera such as Streptococcus (UC), Oribacterium (CD), and TM7x (CD) exhibited bidirectional risk/protective associations within a single IBD subtype; and the TM7x genus was risky for UC and showed bidirectional effects in CD. Other genera (e.g., Fusobacterium, Aggregatibacter) only had unidirectional associations. This study is the first to confirm the causal association between oral microbiota and IBD in East Asian populations, revealing the heterogeneity and "mixed effect" of this association. Identified high-risk and protective oral microbiota taxa provide new insights into IBD etiology and potential targets for clinical precise prevention and treatment.
Additional Links: PMID-41790682
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PubMed:
Citation:
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@article {pmid41790682,
year = {2026},
author = {Xie, RX and Ci, XY and Xue, YB and Liu, M and Zhang, MJ},
title = {Association between oral microbiota and inflammatory bowel disease: A 2-sample Mendelian randomization study in East Asian populations.},
journal = {Medicine},
volume = {105},
number = {10},
pages = {e47909},
doi = {10.1097/MD.0000000000047909},
pmid = {41790682},
issn = {1536-5964},
mesh = {Humans ; Mendelian Randomization Analysis ; Polymorphism, Single Nucleotide ; Genome-Wide Association Study ; Asia, Eastern/epidemiology ; *Microbiota/genetics ; *Crohn Disease/microbiology/genetics ; *Mouth/microbiology ; Asian People/genetics ; *Inflammatory Bowel Diseases/microbiology/genetics/epidemiology ; *Colitis, Ulcerative/microbiology/genetics/epidemiology ; Saliva/microbiology ; Male ; Female ; East Asian People ; },
abstract = {Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is increasingly prevalent in East Asia. Its pathogenesis is linked to microbiota dysbiosis via the oral-gut axis, but population-specific causal evidence remains scarce. This study aimed to clarify the causal associations between oral microbiota and UC/CD in East Asian populations using Mendelian randomization (MR), providing evidence for IBD etiology and precise prevention/treatment. A 2-sample MR approach was adopted, using genome-wide association study data of East Asian populations. Single nucleotide polymorphisms associated with tongue dorsum and salivary microbiota were selected as instrumental variables after rigorous screening (F-statistic > 10, linkage disequilibrium R2 = 0.001). Inverse variance weighted was the primary analysis method, supplemented by sensitivity tests (MR-PRESSO, MR-Egger intercept test, etc) and Benjamini-Hochberg multiple testing correction (false discovery rate < 0.05). A total of 82 oral microbiota taxa (22 families, 35 genera) were significantly causally associated with UC (FDR < 0.05), and 21 taxa (10 families, 12 genera) with CD (FDR < 0.05). High-risk taxa included Aggregatibacter and Streptococcus (OR > 1), while protective taxa included Fusobacterium_periodonticum_C_mgs_3022 and TM7x_unclassified_mgs_1084 (OR < 1). A distinct "mixed effect" was identified: the Streptococcus genus was risky for UC but protective for CD; genera such as Streptococcus (UC), Oribacterium (CD), and TM7x (CD) exhibited bidirectional risk/protective associations within a single IBD subtype; and the TM7x genus was risky for UC and showed bidirectional effects in CD. Other genera (e.g., Fusobacterium, Aggregatibacter) only had unidirectional associations. This study is the first to confirm the causal association between oral microbiota and IBD in East Asian populations, revealing the heterogeneity and "mixed effect" of this association. Identified high-risk and protective oral microbiota taxa provide new insights into IBD etiology and potential targets for clinical precise prevention and treatment.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Mendelian Randomization Analysis
Polymorphism, Single Nucleotide
Genome-Wide Association Study
Asia, Eastern/epidemiology
*Microbiota/genetics
*Crohn Disease/microbiology/genetics
*Mouth/microbiology
Asian People/genetics
*Inflammatory Bowel Diseases/microbiology/genetics/epidemiology
*Colitis, Ulcerative/microbiology/genetics/epidemiology
Saliva/microbiology
Male
Female
East Asian People
RevDate: 2026-03-06
Beyond the binary: understanding inflammatory bowel disease in the context of HIV-Induced immunodeficiency.
Expert review of clinical immunology [Epub ahead of print].
INTRODUCTION: The coexistence of inflammatory bowel disease(IBD) and human immunodeficiency virus(HIV) represents a clinical paradox in which immune hyperactivity coexists with persistent immunodeficiency. Improved survival with antiretroviral therapy(ART) has led to increasing co-diagnoses, creating complex diagnostic and therapeutic challenges.
AREAS COVERED: A comprehensive literature search of PubMed/MEDLINE, Embase, Scopus, and the Cochrane Library from inception through December 2024 was conducted, supplemented by major gastroenterology and infectious disease conference proceedings through April 2025. This review synthesizes contemporary evidence on epidemiology, immunopathogenesis, clinical presentation, and management of IBD in people living with HIV. Key themes include immune reconstitution and Th17-cell depletion, diagnostic differentiation from infectious and noninfectious mimickers, underutilization of advanced IBD therapies despite emerging safety data, bidirectional interactions between intestinal inflammation and HIV viral dynamics, and clinically relevant ART - IBD interactions requiring multidisciplinary care.
EXPERT OPINION: Accumulating evidence supports the safe and appropriate use of immune-modulating therapies in virologically suppressed HIV-positive patients with IBD, challenging historical risk-averse approaches. Optimal management requires precision-based strategy incorporating CD4[+] cell thresholds, mucosal and inflammatory biomarkers, and individualized risk stratification. Future priorities include standardized diagnostic algorithms, longitudinal registries integrating immunological and virological parameters, and improved access to advanced therapies, moving beyond the traditional autoimmunity - immunodeficiency binary.
Additional Links: PMID-41790596
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PubMed:
Citation:
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@article {pmid41790596,
year = {2026},
author = {Srivastava, H and Sehgal, T and Sharma, V and Narang, H and Berinstein, J and Sood, A and Bishu, S and Goyal, MK},
title = {Beyond the binary: understanding inflammatory bowel disease in the context of HIV-Induced immunodeficiency.},
journal = {Expert review of clinical immunology},
volume = {},
number = {},
pages = {},
doi = {10.1080/1744666X.2026.2642832},
pmid = {41790596},
issn = {1744-8409},
abstract = {INTRODUCTION: The coexistence of inflammatory bowel disease(IBD) and human immunodeficiency virus(HIV) represents a clinical paradox in which immune hyperactivity coexists with persistent immunodeficiency. Improved survival with antiretroviral therapy(ART) has led to increasing co-diagnoses, creating complex diagnostic and therapeutic challenges.
AREAS COVERED: A comprehensive literature search of PubMed/MEDLINE, Embase, Scopus, and the Cochrane Library from inception through December 2024 was conducted, supplemented by major gastroenterology and infectious disease conference proceedings through April 2025. This review synthesizes contemporary evidence on epidemiology, immunopathogenesis, clinical presentation, and management of IBD in people living with HIV. Key themes include immune reconstitution and Th17-cell depletion, diagnostic differentiation from infectious and noninfectious mimickers, underutilization of advanced IBD therapies despite emerging safety data, bidirectional interactions between intestinal inflammation and HIV viral dynamics, and clinically relevant ART - IBD interactions requiring multidisciplinary care.
EXPERT OPINION: Accumulating evidence supports the safe and appropriate use of immune-modulating therapies in virologically suppressed HIV-positive patients with IBD, challenging historical risk-averse approaches. Optimal management requires precision-based strategy incorporating CD4[+] cell thresholds, mucosal and inflammatory biomarkers, and individualized risk stratification. Future priorities include standardized diagnostic algorithms, longitudinal registries integrating immunological and virological parameters, and improved access to advanced therapies, moving beyond the traditional autoimmunity - immunodeficiency binary.},
}
RevDate: 2026-03-06
Saccharomyces cerevisiae 48338 Suppresses Antibiotic-Induced Clostridioides difficile Infection in a Murine Model.
Probiotics and antimicrobial proteins [Epub ahead of print].
Clostridioides difficile infection (CDI) is a major cause of antibiotic-associated diarrhea and colitis, driven by toxin-mediated epithelial injury and inflammation. While antibiotics such as vancomycin remain the primary treatment, they can further disrupt the gut microbiota and promote recurrence. Probiotics, including yeast strains, have emerged as potential adjunctive therapies for mitigating CDI. In this study, several Saccharomyces cerevisiae strains were evaluated for their probiotic potential, and strain 48338 was identified as the most promising candidate based on its gastrointestinal tolerance, auto-aggregation ability, and antioxidant activity. Using a CDI mouse model, we found that treatment with S. cerevisiae 48338 reduced disease severity, as reflected by lower clinical sickness scores. Quantitative PCR analysis confirmed that the expression of the toxin gene tcdA was significantly decreased following 48338 treatment, whereas total C. difficile burden remained unchanged. In addition, 48338 treatment might enhance intestinal barrier integrity by upregulating occludin gene expression and also might attenuate production of pro-inflammatory cytokines, particularly the expression of IL-1β. The strain also increased the proportions of Foxp3[+] regulatory T cells and macrophages in both the spleen and mesenteric lymph nodes, as determined by flow cytometry, suggesting a shift towards an anti-inflammatory immune profile. Collectively, these findings suggest that the primary mechanism by which S. cerevisiae 48338 exerts its protective effect against C. difficile infection is not through direct reduction of C. difficile colonization, but primarily through modulation of the microbiome, host immune response, and maintenance of epithelial cell integrity. This study highlights the potential of yeast-based probiotics as adjunctive agents for the prevention or mitigation of CDI.
Additional Links: PMID-41790425
PubMed:
Citation:
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@article {pmid41790425,
year = {2026},
author = {Kim, E and Kim, H and Lee, M and Kim, B and Kim, B and Kim, H and Kim, D and Kang, D and Shatta, A and Kim, JY and Holzapfel, WH and Yoon, H},
title = {Saccharomyces cerevisiae 48338 Suppresses Antibiotic-Induced Clostridioides difficile Infection in a Murine Model.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {41790425},
issn = {1867-1314},
support = {RS-2025-16070149//National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT)/ ; 202400440001//Handong Global University Research Grants/ ; },
abstract = {Clostridioides difficile infection (CDI) is a major cause of antibiotic-associated diarrhea and colitis, driven by toxin-mediated epithelial injury and inflammation. While antibiotics such as vancomycin remain the primary treatment, they can further disrupt the gut microbiota and promote recurrence. Probiotics, including yeast strains, have emerged as potential adjunctive therapies for mitigating CDI. In this study, several Saccharomyces cerevisiae strains were evaluated for their probiotic potential, and strain 48338 was identified as the most promising candidate based on its gastrointestinal tolerance, auto-aggregation ability, and antioxidant activity. Using a CDI mouse model, we found that treatment with S. cerevisiae 48338 reduced disease severity, as reflected by lower clinical sickness scores. Quantitative PCR analysis confirmed that the expression of the toxin gene tcdA was significantly decreased following 48338 treatment, whereas total C. difficile burden remained unchanged. In addition, 48338 treatment might enhance intestinal barrier integrity by upregulating occludin gene expression and also might attenuate production of pro-inflammatory cytokines, particularly the expression of IL-1β. The strain also increased the proportions of Foxp3[+] regulatory T cells and macrophages in both the spleen and mesenteric lymph nodes, as determined by flow cytometry, suggesting a shift towards an anti-inflammatory immune profile. Collectively, these findings suggest that the primary mechanism by which S. cerevisiae 48338 exerts its protective effect against C. difficile infection is not through direct reduction of C. difficile colonization, but primarily through modulation of the microbiome, host immune response, and maintenance of epithelial cell integrity. This study highlights the potential of yeast-based probiotics as adjunctive agents for the prevention or mitigation of CDI.},
}
RevDate: 2026-03-06
Malondialdehyde Drives a Feed-Forward Reactive Oxygen Species Loop in Pediatric Crohn's Disease.
Digestive diseases and sciences [Epub ahead of print].
PURPOSE: Crohn's disease (CD) is a chronic, relapsing inflammatory bowel disease with multifactorial etiology. Recent studies implicate reactive oxygen species (ROS) in pediatric CD. Expression of malondialdehyde (MDA), a biomarker of oxidative stress, is elevated in inflammatory diseases, including CD. This study aimed to evaluate genes driving ROS production in pediatric CD and MDA's role in shaping downstream gene expression.
METHODS: Using the Search Tag Analyze Resource for NCBI's Gene Expression Omnibus (STARGEO), we performed a tagged meta-analysis of publicly available gene expression data comparing pediatric CD with controls. Differentially expressed genes were restricted to p < 0.05 and absolute experimental log ratio of 0.2 for further analysis with Ingenuity Pathway Analysis (IPA), to explore biologic relationships.
RESULTS: Fifty-two pediatric CD samples and 24 healthy pediatric intestinal samples were identified and analyzed via STARGEO, yielding 1968 genes that met inclusion criteria. DUOX2, MMP3, and NOD2 were significantly upregulated in pediatric CD (log ratios of 2.521, 1.823, 0.524, respectively). Upstream regulators include TNF (z-score 11.195), TGFB1 (5.945), IFNG (9.983), and TLR4 (5.989). MDA was identified as a strongly activated regulator with a z-score of 10.909 and downstream targets including TGFB1, MMP3, TNF, and IL-6.
CONCLUSION: Our findings enhance the current understanding of the role of immune dysregulation, ROS, the gut microbiome, and epithelial barrier dysfunction in pediatric CD. DUOX2 functions as one of the central mediators of ROS-driven dysregulation, with TLR4-driven DUOX2 activity potentially overriding the NOD2 regulation. MDA formation stimulates inflammation and tissue injury, upregulating MMP3, which in turn increases ROS production to generate more MDA. This feed-forward inflammatory loop may accelerate fibrosis and chronic inflammation. This meta-analysis provides a preliminary framework of ROS-related gene programs in pediatric CD.
Additional Links: PMID-41790398
PubMed:
Citation:
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@article {pmid41790398,
year = {2026},
author = {Sutton, S and Voskamp, S and Le, K and Hafez, A and Nelson, J and Palomo, P},
title = {Malondialdehyde Drives a Feed-Forward Reactive Oxygen Species Loop in Pediatric Crohn's Disease.},
journal = {Digestive diseases and sciences},
volume = {},
number = {},
pages = {},
pmid = {41790398},
issn = {1573-2568},
abstract = {PURPOSE: Crohn's disease (CD) is a chronic, relapsing inflammatory bowel disease with multifactorial etiology. Recent studies implicate reactive oxygen species (ROS) in pediatric CD. Expression of malondialdehyde (MDA), a biomarker of oxidative stress, is elevated in inflammatory diseases, including CD. This study aimed to evaluate genes driving ROS production in pediatric CD and MDA's role in shaping downstream gene expression.
METHODS: Using the Search Tag Analyze Resource for NCBI's Gene Expression Omnibus (STARGEO), we performed a tagged meta-analysis of publicly available gene expression data comparing pediatric CD with controls. Differentially expressed genes were restricted to p < 0.05 and absolute experimental log ratio of 0.2 for further analysis with Ingenuity Pathway Analysis (IPA), to explore biologic relationships.
RESULTS: Fifty-two pediatric CD samples and 24 healthy pediatric intestinal samples were identified and analyzed via STARGEO, yielding 1968 genes that met inclusion criteria. DUOX2, MMP3, and NOD2 were significantly upregulated in pediatric CD (log ratios of 2.521, 1.823, 0.524, respectively). Upstream regulators include TNF (z-score 11.195), TGFB1 (5.945), IFNG (9.983), and TLR4 (5.989). MDA was identified as a strongly activated regulator with a z-score of 10.909 and downstream targets including TGFB1, MMP3, TNF, and IL-6.
CONCLUSION: Our findings enhance the current understanding of the role of immune dysregulation, ROS, the gut microbiome, and epithelial barrier dysfunction in pediatric CD. DUOX2 functions as one of the central mediators of ROS-driven dysregulation, with TLR4-driven DUOX2 activity potentially overriding the NOD2 regulation. MDA formation stimulates inflammation and tissue injury, upregulating MMP3, which in turn increases ROS production to generate more MDA. This feed-forward inflammatory loop may accelerate fibrosis and chronic inflammation. This meta-analysis provides a preliminary framework of ROS-related gene programs in pediatric CD.},
}
RevDate: 2026-03-06
Clinical development of molecular residual disease (MRD) and multi-cancer early detection (MCED) using liquid biopsy multiomics with artificial intelligence (AI).
International journal of clinical oncology [Epub ahead of print].
BACKGROUND: Early detection of cancer and precise recurrence monitoring remain major unmet needs in oncology. Conventional screening is limited to a few cancer types, leaving nearly half of cancers without established programs. Multi-cancer early detection (MCED) tests based on circulating tumor biomarkers have shown promise, but sensitivity for early-stage remains a challenge. In parallel, detection of molecular residual disease (MRD) using circulating tumor DNA (ctDNA) has emerged as a powerful prognostic and predictive tool, though current assays remain limited in sensitivity and specificity. This study aims to integrate multi-omics data to develop more refined and highly sensitive MCED and MRD assays.
METHODS: This study leverages clinical information and biospecimens from patients with cancer and cancer-naïve individuals. Samples from patients with cancers will be derived from the MONSTAR-SCREEN-3 study, while those from cancer-naïve individuals will be obtained from the Tohoku Medical Megabank Project. Comprehensive analyses will include whole-genome sequencing (WGS), whole-exome sequencing (WES), whole-transcriptome sequencing (WTS), proteomics, metabolomics, and microbiome profiling using stool and saliva. Artificial intelligence (AI)-based multi-omics integration will be performed to develop novel MCED and MRD assays and to evaluate their clinical performance. The primary endpoints are the sensitivity and specificity of MCED and MRD assays.
DISCUSSION: This is the first large-scale study to integrate comprehensive multi-omics profiling with AI for MCED and MRD assay development. The findings are expected to advance precision oncology by improving early diagnosis and recurrence monitoring.
TRIAL REGISTRATION: UMIN000053815, approved by the Institutional Review Board of the National Cancer Center Hospital East.
Additional Links: PMID-41790338
PubMed:
Citation:
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@article {pmid41790338,
year = {2026},
author = {Shibuki, T and Yamashita, R and Hashimoto, T and Fujisawa, T and Imai, M and Yuda, J and Kuwata, T and Misumi, T and Nakamura, Y and Bando, H and Kojima, K and Tokioka, S and Chiba, I and Nakaya, N and Hozawa, A and Koshiba, S and Fuse, N and Saito, S and Shimizu, R and Park, WY and Kinoshita, K and Yoshino, T},
title = {Clinical development of molecular residual disease (MRD) and multi-cancer early detection (MCED) using liquid biopsy multiomics with artificial intelligence (AI).},
journal = {International journal of clinical oncology},
volume = {},
number = {},
pages = {},
pmid = {41790338},
issn = {1437-7772},
support = {23tk0124005h0001//Japan Agency for Medical Research and Development/ ; 24tk0124005h0002//Japan Agency for Medical Research and Development/ ; 25tk0124005h0003//Japan Agency for Medical Research and Development/ ; },
abstract = {BACKGROUND: Early detection of cancer and precise recurrence monitoring remain major unmet needs in oncology. Conventional screening is limited to a few cancer types, leaving nearly half of cancers without established programs. Multi-cancer early detection (MCED) tests based on circulating tumor biomarkers have shown promise, but sensitivity for early-stage remains a challenge. In parallel, detection of molecular residual disease (MRD) using circulating tumor DNA (ctDNA) has emerged as a powerful prognostic and predictive tool, though current assays remain limited in sensitivity and specificity. This study aims to integrate multi-omics data to develop more refined and highly sensitive MCED and MRD assays.
METHODS: This study leverages clinical information and biospecimens from patients with cancer and cancer-naïve individuals. Samples from patients with cancers will be derived from the MONSTAR-SCREEN-3 study, while those from cancer-naïve individuals will be obtained from the Tohoku Medical Megabank Project. Comprehensive analyses will include whole-genome sequencing (WGS), whole-exome sequencing (WES), whole-transcriptome sequencing (WTS), proteomics, metabolomics, and microbiome profiling using stool and saliva. Artificial intelligence (AI)-based multi-omics integration will be performed to develop novel MCED and MRD assays and to evaluate their clinical performance. The primary endpoints are the sensitivity and specificity of MCED and MRD assays.
DISCUSSION: This is the first large-scale study to integrate comprehensive multi-omics profiling with AI for MCED and MRD assay development. The findings are expected to advance precision oncology by improving early diagnosis and recurrence monitoring.
TRIAL REGISTRATION: UMIN000053815, approved by the Institutional Review Board of the National Cancer Center Hospital East.},
}
RevDate: 2026-03-06
Sprayable Lactococcus lactis-Nanocatalyst Gel for Postsurgical Immunomodulation in Preclinical Oral Squamous Cell Carcinoma.
Journal of the American Chemical Society [Epub ahead of print].
Oral squamous cell carcinoma (OSCC) is one of the most prevalent and aggressive head and neck cancers. Emerging evidence shows that distinct microbiomes coexist with tumor and immune cells in the tumor microenvironment (TME), shaping tumor progression and antitumor immunity. Harnessing probiotic-based immune modulation therefore represents a promising strategy to improve postoperative outcomes. Here, we develop a dual-channel sprayable Lactococcus lactis probiotic-nanocatalyst gel (L. lactis@Co4N/C@Gel) to potentiate postoperative immune reconstruction in OSCC. L. lactis can activate antitumor responses through Toll-like and NOD-like receptor pathways. However, its therapeutic benefit is constrained by lactate overproduction, which promotes tumor aggressiveness, immunosuppression, and therapy resistance. The incorporated Co4N/C nanoparticles efficiently scavenge L. lactis-derived lactate, thereby amplifying downstream immune activation. Benefiting from the thixotropic properties of calcium alginate, a sodium alginate solution containing L. lactis and CaCl2 solution containing Co4N/C nanoparticles can be cosprayed to achieve uniform wound coverage and rapid in situ gelation. In an orthotopic OSCC mouse model, L.lactis@Co4N/C@Gel effectively reconstructs postoperative antitumor immunity and markedly suppresses tumor recurrence. These findings highlight a microbiome-nanocatalyst synergistic strategy for improving postoperative immunotherapy in OSCC.
Additional Links: PMID-41790238
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PubMed:
Citation:
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@article {pmid41790238,
year = {2026},
author = {Zhao, S and Liu, B and Shi, Y and Zhou, Z and Chen, S and Saiding, Q and Xu, Q and You, X and Zhen, X and Chen, Q and Zhang, Y and An, S and Tao, N and Ouyang, J and Tao, W},
title = {Sprayable Lactococcus lactis-Nanocatalyst Gel for Postsurgical Immunomodulation in Preclinical Oral Squamous Cell Carcinoma.},
journal = {Journal of the American Chemical Society},
volume = {},
number = {},
pages = {},
doi = {10.1021/jacs.6c01542},
pmid = {41790238},
issn = {1520-5126},
abstract = {Oral squamous cell carcinoma (OSCC) is one of the most prevalent and aggressive head and neck cancers. Emerging evidence shows that distinct microbiomes coexist with tumor and immune cells in the tumor microenvironment (TME), shaping tumor progression and antitumor immunity. Harnessing probiotic-based immune modulation therefore represents a promising strategy to improve postoperative outcomes. Here, we develop a dual-channel sprayable Lactococcus lactis probiotic-nanocatalyst gel (L. lactis@Co4N/C@Gel) to potentiate postoperative immune reconstruction in OSCC. L. lactis can activate antitumor responses through Toll-like and NOD-like receptor pathways. However, its therapeutic benefit is constrained by lactate overproduction, which promotes tumor aggressiveness, immunosuppression, and therapy resistance. The incorporated Co4N/C nanoparticles efficiently scavenge L. lactis-derived lactate, thereby amplifying downstream immune activation. Benefiting from the thixotropic properties of calcium alginate, a sodium alginate solution containing L. lactis and CaCl2 solution containing Co4N/C nanoparticles can be cosprayed to achieve uniform wound coverage and rapid in situ gelation. In an orthotopic OSCC mouse model, L.lactis@Co4N/C@Gel effectively reconstructs postoperative antitumor immunity and markedly suppresses tumor recurrence. These findings highlight a microbiome-nanocatalyst synergistic strategy for improving postoperative immunotherapy in OSCC.},
}
RevDate: 2026-03-06
Rapid Classification of Pantoea spp. via Raman Flow Cytometry.
Analytical chemistry [Epub ahead of print].
Microorganisms play pivotal roles in ecosystems, where precise taxonomic identification is fundamental to understanding and harnessing their functions. Conventional microbial classification, however, relies on pure-culture techniques that suffer from prolonged cultivation cycles, low throughput, high costs, and limited resolution. To address these constraints, we developed an integrated platform combining positive dielectrophoresis-activated Raman-activated cell sorting (pDEP-RACS) with deep ResNet. Using the ecologically versatile and taxonomically challenging genus Pantoea as a model, we constructed a reference Ramanome database by pDEP-RACS that consists of 180 000 single-cell Raman spectra (SCRS) from 12 Pantoea species (22 strains) and two phylogenetically related species and established a classification model by ResNet-18. The model achieved optimal performance 96.9% mean accuracy and 97.3% recall for 24 SCRS colony isolates. Cross-batch validation shows the highest reproducibility in nutrient-starved samples, with 87.9% accuracy postpreprocessing with reduced batch effects. For optimal accuracy (97.6% ± 2.0%), classification accuracy plateaus at >1,500 SCRS of Raman detection depth. In synthetic communities, the model shows ≤3.21% absolute abundance error for species identification. For the rice seed microbiome, a good consistency was observed between Raman-derived Pantoea abundance (34.8%) and 16S rRNA sequencing results (45%). This platform enables species- and strain-level classification of Pantoea spp. cultures, acquiring >7,200 SCRS per hour to facilitate rapid identification in both synthetic microbial communities and field-derived samples.
Additional Links: PMID-41789971
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PubMed:
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@article {pmid41789971,
year = {2026},
author = {Zhang, D and Tian, S and Feng, B and Yang, F and Zhu, P and Wu, Q and Xu, J and Wang, H and Zhang, X},
title = {Rapid Classification of Pantoea spp. via Raman Flow Cytometry.},
journal = {Analytical chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.analchem.6c00276},
pmid = {41789971},
issn = {1520-6882},
abstract = {Microorganisms play pivotal roles in ecosystems, where precise taxonomic identification is fundamental to understanding and harnessing their functions. Conventional microbial classification, however, relies on pure-culture techniques that suffer from prolonged cultivation cycles, low throughput, high costs, and limited resolution. To address these constraints, we developed an integrated platform combining positive dielectrophoresis-activated Raman-activated cell sorting (pDEP-RACS) with deep ResNet. Using the ecologically versatile and taxonomically challenging genus Pantoea as a model, we constructed a reference Ramanome database by pDEP-RACS that consists of 180 000 single-cell Raman spectra (SCRS) from 12 Pantoea species (22 strains) and two phylogenetically related species and established a classification model by ResNet-18. The model achieved optimal performance 96.9% mean accuracy and 97.3% recall for 24 SCRS colony isolates. Cross-batch validation shows the highest reproducibility in nutrient-starved samples, with 87.9% accuracy postpreprocessing with reduced batch effects. For optimal accuracy (97.6% ± 2.0%), classification accuracy plateaus at >1,500 SCRS of Raman detection depth. In synthetic communities, the model shows ≤3.21% absolute abundance error for species identification. For the rice seed microbiome, a good consistency was observed between Raman-derived Pantoea abundance (34.8%) and 16S rRNA sequencing results (45%). This platform enables species- and strain-level classification of Pantoea spp. cultures, acquiring >7,200 SCRS per hour to facilitate rapid identification in both synthetic microbial communities and field-derived samples.},
}
RevDate: 2026-03-06
Insights into bacterial stress adaptation, host interactions, and drug resistance: key findings from the fall 2025 ASM Theobald Smith Society meeting.
mSphere [Epub ahead of print].
The annual fall meeting for the Theobald Smith Society (TSS), the New Jersey Branch of the American Society for Microbiology (ASM), took place in November 2025 at Cooper Medical School of Rowan University in Camden, New Jersey. A total of 72 branch members from across New Jersey participated, including undergraduate and graduate students, postdoctoral trainees, faculty, and professionals from government and industry. This report highlights the scope and diversity of research carried out by TSS members and celebrates their impactful discoveries.
Additional Links: PMID-41789898
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@article {pmid41789898,
year = {2026},
author = {Sharma, N and Singh, M and Radeny, J and Mukherjee, A and Sullivan, RF and Boyd, JM and Carabetta, VJ and Yang, JH and Yadavalli, SS},
title = {Insights into bacterial stress adaptation, host interactions, and drug resistance: key findings from the fall 2025 ASM Theobald Smith Society meeting.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0087825},
doi = {10.1128/msphere.00878-25},
pmid = {41789898},
issn = {2379-5042},
abstract = {The annual fall meeting for the Theobald Smith Society (TSS), the New Jersey Branch of the American Society for Microbiology (ASM), took place in November 2025 at Cooper Medical School of Rowan University in Camden, New Jersey. A total of 72 branch members from across New Jersey participated, including undergraduate and graduate students, postdoctoral trainees, faculty, and professionals from government and industry. This report highlights the scope and diversity of research carried out by TSS members and celebrates their impactful discoveries.},
}
RevDate: 2026-03-06
Gut virome and metabolic associations in patients with acute pancreatitis.
mSystems [Epub ahead of print].
Acute pancreatitis (AP) is a frequent inflammatory disorder with outcomes ranging from mild disease to severe forms marked by infection and organ failure. Gut microenvironment disruption and barrier dysfunction are increasingly recognized as key drivers of AP progression, yet most microbiome studies have focused on bacteria. The gut virome modulates bacterial ecology and host immune responses and remains poorly characterized in AP. We aimed to comprehensively profile virome alterations in AP and evaluate their associations with disease severity, etiology, and clinical parameters. Metagenomic sequencing data from AP patients and healthy controls (HCs) were analyzed using the viromic tools. Viral diversity, taxonomy, functional composition, and predicted viral-host linkages were profiled. Microbial-viral-metabolite networks were constructed, and classification performance was evaluated using random forest models. AP viromes exhibited significantly reduced Shannon and Simpson diversity and distinct β-diversity separation from HCs. AP-enriched phages predominantly targeted Parabacteroides, Escherichia, and Bacteroides, while HC-enriched phages were linked to SCFA-producing commensals. Functional analysis revealed enrichment of replication- and lysis-related auxiliary metabolic genes (AMGs) in AP-enriched viral operational taxonomic units (vOTUs), whereas HC-associated vOTUs carried stability-related functions. Severity- and etiology-stratified analyses indicated consistent enrichment of Peduoviridae infecting Enterobacteriaceae and higher prevalence of eukaryotic viruses in advanced stages. Network analyses revealed denser microbial-viral-metabolite interactions in AP, correlated with hepatobiliary and lipid metabolic markers. A minimal seven-virus panel achieved an AUC of 97.5% for AP classification. AP is characterized by profound gut virome remodeling reflecting disease severity and etiology, with diagnostic and mechanistic relevance for future therapeutic strategies.IMPORTANCEThis study highlights the gut virome as a previously underappreciated component of acute pancreatitis (AP)-associated dysbiosis and suggests that viral communities may influence disease severity and metabolic disturbances beyond bacterial effects alone. By demonstrating the diagnostic potential of virome-based signatures, our findings support expanding microbiome research in AP to include viral components, with implications for improved disease stratification and future therapeutic development.
Additional Links: PMID-41789894
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PubMed:
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@article {pmid41789894,
year = {2026},
author = {Liu, M and Wang, L and Liu, J and Yuan, Q and Zhang, Y and Wu, S and Zhang, Y and Guo, R and Zhang, Y and Lu, T and Yan, Q and Li, S and Xing, G and Dong, B and Zheng, N},
title = {Gut virome and metabolic associations in patients with acute pancreatitis.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0140025},
doi = {10.1128/msystems.01400-25},
pmid = {41789894},
issn = {2379-5077},
abstract = {Acute pancreatitis (AP) is a frequent inflammatory disorder with outcomes ranging from mild disease to severe forms marked by infection and organ failure. Gut microenvironment disruption and barrier dysfunction are increasingly recognized as key drivers of AP progression, yet most microbiome studies have focused on bacteria. The gut virome modulates bacterial ecology and host immune responses and remains poorly characterized in AP. We aimed to comprehensively profile virome alterations in AP and evaluate their associations with disease severity, etiology, and clinical parameters. Metagenomic sequencing data from AP patients and healthy controls (HCs) were analyzed using the viromic tools. Viral diversity, taxonomy, functional composition, and predicted viral-host linkages were profiled. Microbial-viral-metabolite networks were constructed, and classification performance was evaluated using random forest models. AP viromes exhibited significantly reduced Shannon and Simpson diversity and distinct β-diversity separation from HCs. AP-enriched phages predominantly targeted Parabacteroides, Escherichia, and Bacteroides, while HC-enriched phages were linked to SCFA-producing commensals. Functional analysis revealed enrichment of replication- and lysis-related auxiliary metabolic genes (AMGs) in AP-enriched viral operational taxonomic units (vOTUs), whereas HC-associated vOTUs carried stability-related functions. Severity- and etiology-stratified analyses indicated consistent enrichment of Peduoviridae infecting Enterobacteriaceae and higher prevalence of eukaryotic viruses in advanced stages. Network analyses revealed denser microbial-viral-metabolite interactions in AP, correlated with hepatobiliary and lipid metabolic markers. A minimal seven-virus panel achieved an AUC of 97.5% for AP classification. AP is characterized by profound gut virome remodeling reflecting disease severity and etiology, with diagnostic and mechanistic relevance for future therapeutic strategies.IMPORTANCEThis study highlights the gut virome as a previously underappreciated component of acute pancreatitis (AP)-associated dysbiosis and suggests that viral communities may influence disease severity and metabolic disturbances beyond bacterial effects alone. By demonstrating the diagnostic potential of virome-based signatures, our findings support expanding microbiome research in AP to include viral components, with implications for improved disease stratification and future therapeutic development.},
}
RevDate: 2026-03-06
Friend and Foe: Microbes in Orchestrating Immunity and Shaping Infection Dynamics.
ACS infectious diseases [Epub ahead of print].
Microbial communities, or microbiota, are fundamental regulators of host immunity and infection outcomes across diverse body sites, including the gut, skin, respiratory tract, and vagina. Despite advances, infectious diseases remain a global challenge, exacerbated by antimicrobial resistance and emerging pathogens. This review explores the dynamic interplay between microbiota, host immune responses, and pathogens, highlighting how microbial interactions shape immune homeostasis and colonisation resistance. The review discusses therapeutic approaches leveraging probiotics, prebiotics, defined microbial consortia, and fecal microbiota transplantation to enhance resistance against bacterial, viral, fungal, and parasitic infections. These microbiome-based strategies represent promising, sustainable alternatives to conventional antibiotics, offering scalable and mechanism-driven interventions. This review further underscores the potential of microbiota-informed therapies to contribute to effective infectious disease prevention and management while addressing global health challenges.
Additional Links: PMID-41789806
Publisher:
PubMed:
Citation:
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@article {pmid41789806,
year = {2026},
author = {Nair, AV},
title = {Friend and Foe: Microbes in Orchestrating Immunity and Shaping Infection Dynamics.},
journal = {ACS infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1021/acsinfecdis.5c00709},
pmid = {41789806},
issn = {2373-8227},
abstract = {Microbial communities, or microbiota, are fundamental regulators of host immunity and infection outcomes across diverse body sites, including the gut, skin, respiratory tract, and vagina. Despite advances, infectious diseases remain a global challenge, exacerbated by antimicrobial resistance and emerging pathogens. This review explores the dynamic interplay between microbiota, host immune responses, and pathogens, highlighting how microbial interactions shape immune homeostasis and colonisation resistance. The review discusses therapeutic approaches leveraging probiotics, prebiotics, defined microbial consortia, and fecal microbiota transplantation to enhance resistance against bacterial, viral, fungal, and parasitic infections. These microbiome-based strategies represent promising, sustainable alternatives to conventional antibiotics, offering scalable and mechanism-driven interventions. This review further underscores the potential of microbiota-informed therapies to contribute to effective infectious disease prevention and management while addressing global health challenges.},
}
RevDate: 2026-03-07
CmpDate: 2026-03-07
Advances and Ongoing Challenges in Colorectal Cancer.
Chirurgia (Bucharest, Romania : 1990), 121(1):27-42.
Colorectal cancer (CRC) remains a major global health concern, with a rising incidence among younger adults and persistently high mortality in advanced stages, despite significant scientific and technological progress. Its etiology is multifactorial, involving lifestyle factors, genetic susceptibility, chronic inflammation, and gut microbiome dysbiosis. Recent advances in screening, molecular profiling, surgery, and systemic therapies have substantially reshaped CRC management. This narrative review was conducted through a comprehensive literature search of PubMed/MEDLINE, Scopus, and Web of Science databases, covering publications from January 2015 to June 2025. Peer-reviewed articles addressing CRC epidemiology, molecular pathways, screening and diagnostic strategies, surgical management, systemic therapies, and emerging treatment modalities were selected. Evidence was qualitatively synthesized and organized into clinically relevant thematic domains. Recent progress in CRC screening, including advanced endoscopic imaging, fecal DNA testing, and blood-based biomarkers, has improved early detection, although implementation remains uneven. Molecular characterization such as MSI-H/dMMR status, RAS/RAF mutations, HER2 amplification, and consensus molecular subtypes â?" guides prognostic assessment and personalized therapy. Surgical resection remains the cornerstone of curative-intent treatment, with minimally invasive and robotic approaches reducing morbidity while maintaining oncologic safety. Techniques such as complete mesocolic excision and total mesorectal excision, along with multimodal strategies for advanced disease, have expanded therapeutic options. Despite these advances, challenges persist, including therapeutic resistance, tumor heterogeneity, limited immunotherapy efficacy in microsatellite-stable disease, and rising early-onset CRC. Future progress relies on precision medicine, ctDNA-guided monitoring, microbiome-targeted strategies, and optimized surgical selection.
Additional Links: PMID-41789608
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PubMed:
Citation:
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@article {pmid41789608,
year = {2026},
author = {Marginean, SS and Radu, PA and Zurzu, M and Garofil, D and Paic, V and Tigora, A and Bratucu, M and And, FP},
title = {Advances and Ongoing Challenges in Colorectal Cancer.},
journal = {Chirurgia (Bucharest, Romania : 1990)},
volume = {121},
number = {1},
pages = {27-42},
doi = {10.21614/chirurgia.3262},
pmid = {41789608},
issn = {1221-9118},
mesh = {Humans ; *Colorectal Neoplasms/diagnosis/therapy/epidemiology/genetics ; Early Detection of Cancer/methods ; Biomarkers, Tumor/blood ; Prognosis ; Treatment Outcome ; },
abstract = {Colorectal cancer (CRC) remains a major global health concern, with a rising incidence among younger adults and persistently high mortality in advanced stages, despite significant scientific and technological progress. Its etiology is multifactorial, involving lifestyle factors, genetic susceptibility, chronic inflammation, and gut microbiome dysbiosis. Recent advances in screening, molecular profiling, surgery, and systemic therapies have substantially reshaped CRC management. This narrative review was conducted through a comprehensive literature search of PubMed/MEDLINE, Scopus, and Web of Science databases, covering publications from January 2015 to June 2025. Peer-reviewed articles addressing CRC epidemiology, molecular pathways, screening and diagnostic strategies, surgical management, systemic therapies, and emerging treatment modalities were selected. Evidence was qualitatively synthesized and organized into clinically relevant thematic domains. Recent progress in CRC screening, including advanced endoscopic imaging, fecal DNA testing, and blood-based biomarkers, has improved early detection, although implementation remains uneven. Molecular characterization such as MSI-H/dMMR status, RAS/RAF mutations, HER2 amplification, and consensus molecular subtypes â?" guides prognostic assessment and personalized therapy. Surgical resection remains the cornerstone of curative-intent treatment, with minimally invasive and robotic approaches reducing morbidity while maintaining oncologic safety. Techniques such as complete mesocolic excision and total mesorectal excision, along with multimodal strategies for advanced disease, have expanded therapeutic options. Despite these advances, challenges persist, including therapeutic resistance, tumor heterogeneity, limited immunotherapy efficacy in microsatellite-stable disease, and rising early-onset CRC. Future progress relies on precision medicine, ctDNA-guided monitoring, microbiome-targeted strategies, and optimized surgical selection.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Colorectal Neoplasms/diagnosis/therapy/epidemiology/genetics
Early Detection of Cancer/methods
Biomarkers, Tumor/blood
Prognosis
Treatment Outcome
RevDate: 2026-03-08
CmpDate: 2026-03-08
Maternal antenatal health and infant growth outcomes: a Microbiome Understanding in Maternity Study.
Journal of developmental origins of health and disease, 17:e15 pii:S2040174425100378.
The influence of the maternal antenatal environment on infant growth and development beyond the neonatal period is not well understood. This study investigated associations between maternal cardiometabolic health and lifestyle on infant growth during the first year of life. This sub-study of the longitudinal Microbiome Understanding in Maternity Study included 87 mother-infant dyads. Maternal anthropometrics were collected at each trimester. Lifestyle was assessed through the Australian Eating Survey (Trimester T1 and T3) and International Physical Activity Questionnaire (T1, T2 and T3). Infant anthropometrics were measured at birth, 6 weeks, 6 months and 12 months. Changes in weight, weight-for-age z-score, length-for-age z-score, rapid weight gain and conditional weight gain (CWG) were determined. Multiple linear regression was used to assess associations between maternal parameters and infant growth, adjusting for common confounders. Maternal T1 weight (CWG: p = 0.03), T3 weight (CWG: p = 0.03) and GWG (weight z-score change: p = 0.031) were positively associated with increased infant growth from 0 to 6 months. Greater maternal fat mass was associated with increased CWG (p = 0.042) from 6 weeks to 6 months. Higher quality maternal T1 diet was associated with increased infant growth (weight z-score change: p = 0.022, CWG: p = 0.013) from 0 to 12 months. Increased maternal physical activity was associated with increased CWG (p = 0.022) and length z-score change (p = 0.024) from 0 to 12 months in T1, and increased CWG from 6 to 12 months in T2 (p = 0.014) and T3 (p = 0.047). Markers of maternal cardiometabolic health risk and healthier lifestyle were associated with increased infant growth. Further investigation is required to confirm findings and investigate links with future health sequelae.
Additional Links: PMID-41789481
Publisher:
PubMed:
Citation:
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@article {pmid41789481,
year = {2026},
author = {Stevenson, E and Susic, D and Craig, ME and Henry, A and Gow, M},
title = {Maternal antenatal health and infant growth outcomes: a Microbiome Understanding in Maternity Study.},
journal = {Journal of developmental origins of health and disease},
volume = {17},
number = {},
pages = {e15},
doi = {10.1017/S2040174425100378},
pmid = {41789481},
issn = {2040-1752},
mesh = {Humans ; Female ; Pregnancy ; Infant ; Adult ; *Child Development/physiology ; Infant, Newborn ; *Maternal Health/statistics & numerical data ; Longitudinal Studies ; Australia/epidemiology ; Male ; Life Style ; *Microbiota/physiology ; Weight Gain ; },
abstract = {The influence of the maternal antenatal environment on infant growth and development beyond the neonatal period is not well understood. This study investigated associations between maternal cardiometabolic health and lifestyle on infant growth during the first year of life. This sub-study of the longitudinal Microbiome Understanding in Maternity Study included 87 mother-infant dyads. Maternal anthropometrics were collected at each trimester. Lifestyle was assessed through the Australian Eating Survey (Trimester T1 and T3) and International Physical Activity Questionnaire (T1, T2 and T3). Infant anthropometrics were measured at birth, 6 weeks, 6 months and 12 months. Changes in weight, weight-for-age z-score, length-for-age z-score, rapid weight gain and conditional weight gain (CWG) were determined. Multiple linear regression was used to assess associations between maternal parameters and infant growth, adjusting for common confounders. Maternal T1 weight (CWG: p = 0.03), T3 weight (CWG: p = 0.03) and GWG (weight z-score change: p = 0.031) were positively associated with increased infant growth from 0 to 6 months. Greater maternal fat mass was associated with increased CWG (p = 0.042) from 6 weeks to 6 months. Higher quality maternal T1 diet was associated with increased infant growth (weight z-score change: p = 0.022, CWG: p = 0.013) from 0 to 12 months. Increased maternal physical activity was associated with increased CWG (p = 0.022) and length z-score change (p = 0.024) from 0 to 12 months in T1, and increased CWG from 6 to 12 months in T2 (p = 0.014) and T3 (p = 0.047). Markers of maternal cardiometabolic health risk and healthier lifestyle were associated with increased infant growth. Further investigation is required to confirm findings and investigate links with future health sequelae.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
Pregnancy
Infant
Adult
*Child Development/physiology
Infant, Newborn
*Maternal Health/statistics & numerical data
Longitudinal Studies
Australia/epidemiology
Male
Life Style
*Microbiota/physiology
Weight Gain
RevDate: 2026-03-07
CmpDate: 2026-03-07
Analysis of Fusobacterium nucleatum Driven Modulation of c-Myc Pathways in Oral Carcinogenesis.
F1000Research, 15:176.
OBJECTIVE: To evaluate the association between Fusobacterium nucleatum and c-Myc expression in Oral Potentially Malignant Disorders (OPMDs) and Oral Squamous Cell Carcinoma (OSCC) and to explore its potential role in oral carcinogenesis.
MATERIALS AND METHODS: A total of 32 histopathologically confirmed cases (18 OPMDs and 14 OSCC) were analyzed. Anaerobic cultures and polymerase chain reaction (PCR) were used to detect F. nucleatum. Immunohistochemistry (IHC) was performed to assess c-Myc expression. Statistical analysis was conducted using Mann-Whitney and Chi-square tests, with p < 0.05 considered significant.
RESULTS: F. nucleatum was detected in eight OSCC and two OPMD cases, with higher colony counts in OSCC. All samples were positive for c-Myc, but their expression levels varied. In OPMDs, positivity was mainly observed in the basal and suprabasal epithelial layers, whereas OSCC showed both peripheral and central tumor cell localization. F. nucleatum-positive OSCC cases demonstrated strong nuclear c-Myc staining (50-75% positive cells). Tobacco habits, particularly combined smoking and smokeless use, were more common in F. nucleatum-positive OSCC cases.
CONCLUSION: F. nucleatum colonization correlates with increased c-Myc expression in OPMDs and OSCC, supporting its possible role in microbially driven oral carcinogenesis. These findings suggest its potential as a prognostic biomarker and a therapeutic target.
Additional Links: PMID-41789431
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Citation:
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@article {pmid41789431,
year = {2026},
author = {Priya, C and Jain, A and Shetty, DC and Pai Khot, AJ and Yadav, S and Jain, M and Gulati, N and Almalki, SA and Gowdar, IM},
title = {Analysis of Fusobacterium nucleatum Driven Modulation of c-Myc Pathways in Oral Carcinogenesis.},
journal = {F1000Research},
volume = {15},
number = {},
pages = {176},
pmid = {41789431},
issn = {2046-1402},
mesh = {Humans ; *Fusobacterium nucleatum/physiology ; *Mouth Neoplasms/microbiology/metabolism/pathology ; *Proto-Oncogene Proteins c-myc/metabolism ; Female ; Male ; *Carcinogenesis/metabolism/pathology ; Middle Aged ; Aged ; *Carcinoma, Squamous Cell/microbiology/metabolism/pathology ; Adult ; Fusobacterium Infections ; Signal Transduction ; },
abstract = {OBJECTIVE: To evaluate the association between Fusobacterium nucleatum and c-Myc expression in Oral Potentially Malignant Disorders (OPMDs) and Oral Squamous Cell Carcinoma (OSCC) and to explore its potential role in oral carcinogenesis.
MATERIALS AND METHODS: A total of 32 histopathologically confirmed cases (18 OPMDs and 14 OSCC) were analyzed. Anaerobic cultures and polymerase chain reaction (PCR) were used to detect F. nucleatum. Immunohistochemistry (IHC) was performed to assess c-Myc expression. Statistical analysis was conducted using Mann-Whitney and Chi-square tests, with p < 0.05 considered significant.
RESULTS: F. nucleatum was detected in eight OSCC and two OPMD cases, with higher colony counts in OSCC. All samples were positive for c-Myc, but their expression levels varied. In OPMDs, positivity was mainly observed in the basal and suprabasal epithelial layers, whereas OSCC showed both peripheral and central tumor cell localization. F. nucleatum-positive OSCC cases demonstrated strong nuclear c-Myc staining (50-75% positive cells). Tobacco habits, particularly combined smoking and smokeless use, were more common in F. nucleatum-positive OSCC cases.
CONCLUSION: F. nucleatum colonization correlates with increased c-Myc expression in OPMDs and OSCC, supporting its possible role in microbially driven oral carcinogenesis. These findings suggest its potential as a prognostic biomarker and a therapeutic target.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Fusobacterium nucleatum/physiology
*Mouth Neoplasms/microbiology/metabolism/pathology
*Proto-Oncogene Proteins c-myc/metabolism
Female
Male
*Carcinogenesis/metabolism/pathology
Middle Aged
Aged
*Carcinoma, Squamous Cell/microbiology/metabolism/pathology
Adult
Fusobacterium Infections
Signal Transduction
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