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ESP: PubMed Auto Bibliography 25 Feb 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: 2026-02-23
CmpDate: 2026-02-23
Neutrophil extracellular traps in gynecological disease: pathogenic mechanisms and therapeutic opportunities.
Frontiers in medicine, 13:1710628.
Gynecologic disorders, including infections, sterile inflammatory diseases, endocrine abnormalities, and malignancies, share a common signature of dysregulated immunity within a uniquely hormone-responsive reproductive tract. Neutrophil extracellular traps (NETs) are increasingly recognized as central effectors at this interface of innate immunity, endocrine signaling, tissue remodeling, and thrombosis. In this review, we first outline the mechanistic basis of NET formation and emphasize how the cyclical anatomy, fluctuating sex hormones, and regional microbiota of the female reproductive tract shape NET induction, localization, and clearance. We then synthesize evidence across disease spectra. In infectious conditions such as pelvic inflammatory disease, genital tuberculosis, and vaginal dysbiosis, NETs confine pathogens but also drive epithelial injury, fibrosis, and infertility. In sterile inflammatory and endocrine-related disorders, including endometriosis, polycystic ovary syndrome, premature ovarian insufficiency, and primary dysmenorrhea, NET-associated oxidative stress, inflammasome activation, and profibrotic signaling link hormonal and metabolic imbalance to chronic pain and organ dysfunction. In gynecologic cancers, NETs promote tumor cell adhesion, invasion, immune escape, and thromboembolic complications within hormone-conditioned microenvironments, while circulating and tissue NET markers, as well as NET-related gene and lncRNA signatures, hold diagnostic and prognostic value. Finally, we discuss how biomaterial-based strategies in vaginal reconstruction exploit antimicrobial NET functions yet risk excessive fibrosis if NETs are not tightly controlled. Across these contexts, we highlight an emerging NET-sex hormone axis and propose endocrine-aware, biomarker-guided strategies that combine NET-targeting agents with hormonal and microbiome-based interventions to achieve more precise diagnosis, risk stratification, and therapy for gynecologic diseases.
Additional Links: PMID-41728621
PubMed:
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@article {pmid41728621,
year = {2026},
author = {Wu, M and Ding, J and Zhang, X},
title = {Neutrophil extracellular traps in gynecological disease: pathogenic mechanisms and therapeutic opportunities.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1710628},
pmid = {41728621},
issn = {2296-858X},
abstract = {Gynecologic disorders, including infections, sterile inflammatory diseases, endocrine abnormalities, and malignancies, share a common signature of dysregulated immunity within a uniquely hormone-responsive reproductive tract. Neutrophil extracellular traps (NETs) are increasingly recognized as central effectors at this interface of innate immunity, endocrine signaling, tissue remodeling, and thrombosis. In this review, we first outline the mechanistic basis of NET formation and emphasize how the cyclical anatomy, fluctuating sex hormones, and regional microbiota of the female reproductive tract shape NET induction, localization, and clearance. We then synthesize evidence across disease spectra. In infectious conditions such as pelvic inflammatory disease, genital tuberculosis, and vaginal dysbiosis, NETs confine pathogens but also drive epithelial injury, fibrosis, and infertility. In sterile inflammatory and endocrine-related disorders, including endometriosis, polycystic ovary syndrome, premature ovarian insufficiency, and primary dysmenorrhea, NET-associated oxidative stress, inflammasome activation, and profibrotic signaling link hormonal and metabolic imbalance to chronic pain and organ dysfunction. In gynecologic cancers, NETs promote tumor cell adhesion, invasion, immune escape, and thromboembolic complications within hormone-conditioned microenvironments, while circulating and tissue NET markers, as well as NET-related gene and lncRNA signatures, hold diagnostic and prognostic value. Finally, we discuss how biomaterial-based strategies in vaginal reconstruction exploit antimicrobial NET functions yet risk excessive fibrosis if NETs are not tightly controlled. Across these contexts, we highlight an emerging NET-sex hormone axis and propose endocrine-aware, biomarker-guided strategies that combine NET-targeting agents with hormonal and microbiome-based interventions to achieve more precise diagnosis, risk stratification, and therapy for gynecologic diseases.},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
Decrypting molecular mechanism of heat stress tolerance in rice to tackle climate change challenges through recent approaches.
Frontiers in plant science, 16:1722694.
Rice (Oryza sativa) is one of the world's most important cereal crops, contributing to food and financial security, particularly in developing countries. High temperature due to climate change seriously threatens sustainable rice production. Rice crops are adversely affected by heat stress at the morphological, physiological, and molecular levels, resulting in reduced yield and poor grain quality. Rice is highly sensitive to heat during the reproductive phase, causing pollen sterility, impaired pollen dehiscence, pollen germination, and tube growth, ultimately drastically reducing spikelet sterility and yield. High temperature also promotes the accumulation of reactive oxygen species in plant cells, resulting in multiple adverse effects, including damage to chloroplasts and cell membranes, inactivation of photosystems, reduced Rubisco activity, and impaired production of photoassimilates. In this review, we have synthesized the current knowledge on the effects of heat stress on rice and summarized QTLs, genes, and regulatory pathways underlying thermotolerance. We further evaluate conventional breeding, transgenics, and diverse omics-based strategies to breed high-yielding, heat-tolerant rice varieties. The precise molecular insights gained through various omics approaches are expected to advance our understanding of the intricate nature of heat stress tolerance in rice. Additionally, we highlight the emerging roles of microbiome, high-throughput phenotyping technologies, and artificial intelligence as promising tools for accelerating the development of heat-resilient rice.
Additional Links: PMID-41728192
PubMed:
Citation:
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@article {pmid41728192,
year = {2025},
author = {Kumar, N and Khatibi, SMH and Sharma, D and Azeem, F and Koutu, GK and Ali, J},
title = {Decrypting molecular mechanism of heat stress tolerance in rice to tackle climate change challenges through recent approaches.},
journal = {Frontiers in plant science},
volume = {16},
number = {},
pages = {1722694},
pmid = {41728192},
issn = {1664-462X},
abstract = {Rice (Oryza sativa) is one of the world's most important cereal crops, contributing to food and financial security, particularly in developing countries. High temperature due to climate change seriously threatens sustainable rice production. Rice crops are adversely affected by heat stress at the morphological, physiological, and molecular levels, resulting in reduced yield and poor grain quality. Rice is highly sensitive to heat during the reproductive phase, causing pollen sterility, impaired pollen dehiscence, pollen germination, and tube growth, ultimately drastically reducing spikelet sterility and yield. High temperature also promotes the accumulation of reactive oxygen species in plant cells, resulting in multiple adverse effects, including damage to chloroplasts and cell membranes, inactivation of photosystems, reduced Rubisco activity, and impaired production of photoassimilates. In this review, we have synthesized the current knowledge on the effects of heat stress on rice and summarized QTLs, genes, and regulatory pathways underlying thermotolerance. We further evaluate conventional breeding, transgenics, and diverse omics-based strategies to breed high-yielding, heat-tolerant rice varieties. The precise molecular insights gained through various omics approaches are expected to advance our understanding of the intricate nature of heat stress tolerance in rice. Additionally, we highlight the emerging roles of microbiome, high-throughput phenotyping technologies, and artificial intelligence as promising tools for accelerating the development of heat-resilient rice.},
}
RevDate: 2026-02-23
Editorial: Impact of oral and gut microbiome on health and diseases.
Frontiers in cellular and infection microbiology, 16:1792511.
Additional Links: PMID-41728113
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Citation:
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@article {pmid41728113,
year = {2026},
author = {Das, S and Clayton, JB and Sarkar, S},
title = {Editorial: Impact of oral and gut microbiome on health and diseases.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1792511},
doi = {10.3389/fcimb.2026.1792511},
pmid = {41728113},
issn = {2235-2988},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
Peri-implantitis biofilm from explanted implants in Korean patients: microbial and functional profiling.
Frontiers in cellular and infection microbiology, 16:1768841.
Peri-implantitis is an inflammatory disease affecting tissues surrounding dental implants, with microbial biofilms recognized as the primary etiological factor. However, most previous studies analyzed samples from peri-implant pockets, and research on biofilms directly attached to explanted implant surfaces remains limited. This study compared the microbial composition and functional characteristics of biofilms from explanted implant surfaces in peri-implantitis cases with subgingival plaque from healthy controls. A total of 41 samples (peri-implantitis n=19, healthy controls n=22) were obtained from the Apple Tree Oral Biobank. The V3-V4 region of 16S rRNA gene was sequenced using Illumina MiSeq, ASVs were generated using DADA2, and taxonomic assignment was performed using SILVA database (v138.1). Alpha and beta diversity analyses were conducted, and functional potential was predicted using PICRUSt2. The peri-implantitis group showed significantly higher Simpson index (p=0.0086) and phylogenetic diversity (p<0.0001), with distinct clustering separation between groups. Beyond well-known periodontal pathogens (Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Filifactor alocis), the peri-implantitis group exhibited significant increases in sulfate-reducing bacteria (Desulfobulbus, Desulfovibrio) and emerging pathogens ([Eubacterium] nodatum group, [Eubacterium] saphenum group, Phocaeicola abscessus, Pseudoramibacter alactolyticus, Pyramidobacter). Health-associated bacteria (Corynebacterium, Neisseria, Capnocytophaga, Lautropia) were decreased. Functional analysis revealed enrichment in LPS biosynthesis, sulfur metabolism, iron acquisition, and amino acid degradation pathways, while carbohydrate metabolism was decreased. This study demonstrates that diverse emerging pathogens, including sulfate-reducing bacteria, are associated with peri-implantitis biofilms in explanted implant surface biofilms, contributing to expanded understanding of peri-implantitis etiology and development of candidate biomarkers.
Additional Links: PMID-41728109
PubMed:
Citation:
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@article {pmid41728109,
year = {2026},
author = {Eom, JH and Cho, MY and Kim, JW and Kim, Y and Yang, SJ and Hwang, J and Lee, D and Kim, HS and Baek, H and Kim, YY},
title = {Peri-implantitis biofilm from explanted implants in Korean patients: microbial and functional profiling.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1768841},
pmid = {41728109},
issn = {2235-2988},
mesh = {*Biofilms/growth & development ; Humans ; *Peri-Implantitis/microbiology ; RNA, Ribosomal, 16S/genetics ; Phylogeny ; Middle Aged ; *Dental Implants/microbiology ; Male ; *Bacteria/classification/genetics/isolation & purification ; Female ; Republic of Korea ; Microbiota ; Aged ; Adult ; DNA, Bacterial/genetics ; Dental Plaque/microbiology ; },
abstract = {Peri-implantitis is an inflammatory disease affecting tissues surrounding dental implants, with microbial biofilms recognized as the primary etiological factor. However, most previous studies analyzed samples from peri-implant pockets, and research on biofilms directly attached to explanted implant surfaces remains limited. This study compared the microbial composition and functional characteristics of biofilms from explanted implant surfaces in peri-implantitis cases with subgingival plaque from healthy controls. A total of 41 samples (peri-implantitis n=19, healthy controls n=22) were obtained from the Apple Tree Oral Biobank. The V3-V4 region of 16S rRNA gene was sequenced using Illumina MiSeq, ASVs were generated using DADA2, and taxonomic assignment was performed using SILVA database (v138.1). Alpha and beta diversity analyses were conducted, and functional potential was predicted using PICRUSt2. The peri-implantitis group showed significantly higher Simpson index (p=0.0086) and phylogenetic diversity (p<0.0001), with distinct clustering separation between groups. Beyond well-known periodontal pathogens (Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Filifactor alocis), the peri-implantitis group exhibited significant increases in sulfate-reducing bacteria (Desulfobulbus, Desulfovibrio) and emerging pathogens ([Eubacterium] nodatum group, [Eubacterium] saphenum group, Phocaeicola abscessus, Pseudoramibacter alactolyticus, Pyramidobacter). Health-associated bacteria (Corynebacterium, Neisseria, Capnocytophaga, Lautropia) were decreased. Functional analysis revealed enrichment in LPS biosynthesis, sulfur metabolism, iron acquisition, and amino acid degradation pathways, while carbohydrate metabolism was decreased. This study demonstrates that diverse emerging pathogens, including sulfate-reducing bacteria, are associated with peri-implantitis biofilms in explanted implant surface biofilms, contributing to expanded understanding of peri-implantitis etiology and development of candidate biomarkers.},
}
MeSH Terms:
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hide MeSH Terms
*Biofilms/growth & development
Humans
*Peri-Implantitis/microbiology
RNA, Ribosomal, 16S/genetics
Phylogeny
Middle Aged
*Dental Implants/microbiology
Male
*Bacteria/classification/genetics/isolation & purification
Female
Republic of Korea
Microbiota
Aged
Adult
DNA, Bacterial/genetics
Dental Plaque/microbiology
RevDate: 2026-02-23
CmpDate: 2026-02-23
Drought-tolerant rhizobacterial consortia enhance grapevine growth and tolerance to water deficit.
Frontiers in plant science, 17:1735733.
In both natural ecosystems and in agroecosystems, Plant Growth-Promoting Rhizobacteria (PGPR) significantly contribute to plant development and stress mitigation through diverse mechanisms. In recent times, their application as microbial biostimulants (MBs) has gained attention, particularly for alleviating drought stress, which increasingly threatens grapevine productivity in both modern and traditional wine-growing regions. Despite this interest, functionally validated and biosafe PGPR consortia specifically tailored for grapevine remain limited. This study isolated drought-tolerant PGPRs from grapevine rhizosphere cultivated under contrasting environmental conditions and experiencing midday leaf water potentials between -1.3 and -1.4 MPa. The isolates were ranked according to their Plant Growth-Promoting Traits (PGPTs), and whole-genome sequencing was performed on the nine most promising strains to evaluate their functional potential and biosafety. Such functional traits are known to influence plant performance, providing a conceptual basis for evaluating their effects on grapevine growth. Based on their complementary PGPT profiles and demonstrated compatibility, these strains were assembled into four bacterial consortia (BC1-BC4). The consortia were applied by root dipping and soil inoculation to one-year-old grapevines subjected to progressive drought stress, in order to assess their potential synergistic effects on plant growth. Treated vines were compared to a non-inoculated control (NI). Results indicate that while BC1 and BC2 did not significantly impact shoot growth, BC3 and partially also BC4 increased shoot length by 35.5% and 26.5%, respectively, compared to NI. Notably, BC3 enhanced shoot elongation during the early phase under well-watered conditions, whereas BC4 conferred greater benefits under water deficit. After five days of suspended irrigation, BC4-treated vines maintained higher photosynthetic activity and stomatal conductance compared to all other treatments, which, displayed almost complete stomatal closure. This response may be linked to the enrichment of indole-3-acetic acid-producing and exopolysaccharide-forming strains, which are known to modulate plant growth and water status. Finally, both BC3 and BC4 promoted greater root biomass by the end of the pot trial. Overall, the results highlight the potential of rationally tailored PGPR consortia to enhance grapevine growth under both optimal and drought conditions, supporting their application as context-specific MBs for sustainable viticulture.
Additional Links: PMID-41728002
PubMed:
Citation:
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@article {pmid41728002,
year = {2026},
author = {Canavera, G and Bellotti, G and Tiwari, H and Frioni, T and Puglisi, E},
title = {Drought-tolerant rhizobacterial consortia enhance grapevine growth and tolerance to water deficit.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1735733},
pmid = {41728002},
issn = {1664-462X},
abstract = {In both natural ecosystems and in agroecosystems, Plant Growth-Promoting Rhizobacteria (PGPR) significantly contribute to plant development and stress mitigation through diverse mechanisms. In recent times, their application as microbial biostimulants (MBs) has gained attention, particularly for alleviating drought stress, which increasingly threatens grapevine productivity in both modern and traditional wine-growing regions. Despite this interest, functionally validated and biosafe PGPR consortia specifically tailored for grapevine remain limited. This study isolated drought-tolerant PGPRs from grapevine rhizosphere cultivated under contrasting environmental conditions and experiencing midday leaf water potentials between -1.3 and -1.4 MPa. The isolates were ranked according to their Plant Growth-Promoting Traits (PGPTs), and whole-genome sequencing was performed on the nine most promising strains to evaluate their functional potential and biosafety. Such functional traits are known to influence plant performance, providing a conceptual basis for evaluating their effects on grapevine growth. Based on their complementary PGPT profiles and demonstrated compatibility, these strains were assembled into four bacterial consortia (BC1-BC4). The consortia were applied by root dipping and soil inoculation to one-year-old grapevines subjected to progressive drought stress, in order to assess their potential synergistic effects on plant growth. Treated vines were compared to a non-inoculated control (NI). Results indicate that while BC1 and BC2 did not significantly impact shoot growth, BC3 and partially also BC4 increased shoot length by 35.5% and 26.5%, respectively, compared to NI. Notably, BC3 enhanced shoot elongation during the early phase under well-watered conditions, whereas BC4 conferred greater benefits under water deficit. After five days of suspended irrigation, BC4-treated vines maintained higher photosynthetic activity and stomatal conductance compared to all other treatments, which, displayed almost complete stomatal closure. This response may be linked to the enrichment of indole-3-acetic acid-producing and exopolysaccharide-forming strains, which are known to modulate plant growth and water status. Finally, both BC3 and BC4 promoted greater root biomass by the end of the pot trial. Overall, the results highlight the potential of rationally tailored PGPR consortia to enhance grapevine growth under both optimal and drought conditions, supporting their application as context-specific MBs for sustainable viticulture.},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
Micro-nanobubble oxygenation irrigation ameliorates saline-alkali soil properties, cotton physiology, and yield under different salt stress levels.
Frontiers in plant science, 17:1727907.
BACKGROUND: Addressing soil saline-alkalization is crucial for sustaining cotton production in the arid regions of Xinjiang. This study investigates the efficacy of Micro-Nanobubble oxygenated irrigation (MNBs) compared with conventional flooding (CF) in ameliorating saline-alkali soil and enhancing cotton growth.
METHODS: A field microplot experiment was conducted across four soil salinity levels (0, 3%, 6%, and 9%, with sulfate as the dominant salt).
RESULTS: The results demonstrated that MNBs effectively reduced topsoil (0~20 cm) salinity and mitigated its associated alkalinity stress by facilitating salt leaching into deeper soil layers (20~60 cm). This irrigation method also significantly improved soil enzyme activities and altered ionic dynamics toward a more favorable balance. Moreover, MNBs enhanced soil bacterial diversity, enriched beneficial phyla such as Proteobacteria and Actinobacteria, and modulated fungal genera including Alternaria and Fusarium, suggesting an improved rhizospheric microbiome. In terms of cotton physiology, Micro-nanobubble oxygenation irrigation significantly enhanced the activities of superoxide dismutase (SOD) and peroxidase (POD) in cotton leaves by 15.84% to 40.69% and 10.11% to 33.63%, respectively, while reducing malondialdehyde (MDA) content by 28.22% to 42.11%, thereby alleviating saline-alkali stress-induced oxidative damage. Additionally, MNBs promoted root growth by 0.96% to 29.90%, increased the leaf area index by 18.68% to 25.50%, and enhanced dry matter accumulation by 6.82% to 33.29%. Ultimately, these improvements led to a higher seed cotton yield. Compared with conventional flooding (CF), the MNBs treatment increased seed cotton yield by 33.78%, 35.93%, 47.11%, and 52.31% across the four salinity levels, respectively.
CONCLUSION: In conclusion, micro-nanobubble oxygenation irrigation represents an effective strategy for rehabilitating saline-alkali soils and promoting sustainable agricultural development in arid areas.
Additional Links: PMID-41728000
PubMed:
Citation:
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@article {pmid41728000,
year = {2026},
author = {Yang, Y and Bian, Q and Feng, Y and Wang, Z and Fu, Y and Wei, Y and Zhu, J},
title = {Micro-nanobubble oxygenation irrigation ameliorates saline-alkali soil properties, cotton physiology, and yield under different salt stress levels.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1727907},
pmid = {41728000},
issn = {1664-462X},
abstract = {BACKGROUND: Addressing soil saline-alkalization is crucial for sustaining cotton production in the arid regions of Xinjiang. This study investigates the efficacy of Micro-Nanobubble oxygenated irrigation (MNBs) compared with conventional flooding (CF) in ameliorating saline-alkali soil and enhancing cotton growth.
METHODS: A field microplot experiment was conducted across four soil salinity levels (0, 3%, 6%, and 9%, with sulfate as the dominant salt).
RESULTS: The results demonstrated that MNBs effectively reduced topsoil (0~20 cm) salinity and mitigated its associated alkalinity stress by facilitating salt leaching into deeper soil layers (20~60 cm). This irrigation method also significantly improved soil enzyme activities and altered ionic dynamics toward a more favorable balance. Moreover, MNBs enhanced soil bacterial diversity, enriched beneficial phyla such as Proteobacteria and Actinobacteria, and modulated fungal genera including Alternaria and Fusarium, suggesting an improved rhizospheric microbiome. In terms of cotton physiology, Micro-nanobubble oxygenation irrigation significantly enhanced the activities of superoxide dismutase (SOD) and peroxidase (POD) in cotton leaves by 15.84% to 40.69% and 10.11% to 33.63%, respectively, while reducing malondialdehyde (MDA) content by 28.22% to 42.11%, thereby alleviating saline-alkali stress-induced oxidative damage. Additionally, MNBs promoted root growth by 0.96% to 29.90%, increased the leaf area index by 18.68% to 25.50%, and enhanced dry matter accumulation by 6.82% to 33.29%. Ultimately, these improvements led to a higher seed cotton yield. Compared with conventional flooding (CF), the MNBs treatment increased seed cotton yield by 33.78%, 35.93%, 47.11%, and 52.31% across the four salinity levels, respectively.
CONCLUSION: In conclusion, micro-nanobubble oxygenation irrigation represents an effective strategy for rehabilitating saline-alkali soils and promoting sustainable agricultural development in arid areas.},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
Deciphering the interplay between fruit-associated metabolites and bacterial communities across four distinct mango cultivars.
Frontiers in plant science, 17:1754579.
Mango (Mangifera indica L.) fruit characteristics and health are strongly determined by their biochemical profiles and fruit-associated microbiome composition. However, the cultivar-specific interplay between the mango fruit metabolome and microbiome remains elusive. Here, we tracked differential changes in fruit metabolites and bacterial community composition in four economically important mango cultivars in China: Qingmang (QM), Yumang (YM), Tainong (TN), and Aomang (AM). Using untargeted metabolomics with liquid chromatography-mass spectrometry and high-throughput amplicon sequencing of bacterial 16S rRNA, we identified distinct metabolic profiles and the enrichment of a specific subset of microbiota unique to each cultivar. Different metabolites associated with nitrogen and carbon metabolism, biosynthesis of amino acids, secondary metabolites, and flavonoids were differentially abundant in the four mango cultivars. These classes of metabolites have been previously linked to fruit development, color, antioxidant capacity, and stress resistance. Importantly, significant positive correlations were found between specific bacterial taxa, such as Alcanivorax, Alistipes, Curtobacterium, Rikenella, Thiopseudomonas, Rikenella, and Vogesella and the accumulation of the metabolites ornithine, L-arginine, tricetin, casoxin D, mhppa sulfate, sorbitan palmitate, meconic acid and rengyoside B. These results indicate the critical role of mango cultivars in shaping the fruit-specific microbiomes and metabolites. Our findings provide a foundational understanding of mango fruit holobionts and offer novel insights into metabolic and microbial networks for developing strategies to enhance fruit quality and postharvest management.
Additional Links: PMID-41727994
PubMed:
Citation:
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@article {pmid41727994,
year = {2026},
author = {Zhang, C and Wan, R and Nong, S and Huang, W and Al-Rejaie, SS and Wang, F and Yang, Z and Zhu, Z and Mohany, M},
title = {Deciphering the interplay between fruit-associated metabolites and bacterial communities across four distinct mango cultivars.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1754579},
pmid = {41727994},
issn = {1664-462X},
abstract = {Mango (Mangifera indica L.) fruit characteristics and health are strongly determined by their biochemical profiles and fruit-associated microbiome composition. However, the cultivar-specific interplay between the mango fruit metabolome and microbiome remains elusive. Here, we tracked differential changes in fruit metabolites and bacterial community composition in four economically important mango cultivars in China: Qingmang (QM), Yumang (YM), Tainong (TN), and Aomang (AM). Using untargeted metabolomics with liquid chromatography-mass spectrometry and high-throughput amplicon sequencing of bacterial 16S rRNA, we identified distinct metabolic profiles and the enrichment of a specific subset of microbiota unique to each cultivar. Different metabolites associated with nitrogen and carbon metabolism, biosynthesis of amino acids, secondary metabolites, and flavonoids were differentially abundant in the four mango cultivars. These classes of metabolites have been previously linked to fruit development, color, antioxidant capacity, and stress resistance. Importantly, significant positive correlations were found between specific bacterial taxa, such as Alcanivorax, Alistipes, Curtobacterium, Rikenella, Thiopseudomonas, Rikenella, and Vogesella and the accumulation of the metabolites ornithine, L-arginine, tricetin, casoxin D, mhppa sulfate, sorbitan palmitate, meconic acid and rengyoside B. These results indicate the critical role of mango cultivars in shaping the fruit-specific microbiomes and metabolites. Our findings provide a foundational understanding of mango fruit holobionts and offer novel insights into metabolic and microbial networks for developing strategies to enhance fruit quality and postharvest management.},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
Effects of T2-high asthma heterogeneity and inhaled corticosteroid on airway and metabolic profiles: A multi-omic approach.
Journal of translational internal medicine, 14(1):79-95.
BACKGROUND AND OBJECTIVES: Asthma represents a heterogeneous chronic respiratory condition. Type 2 (T2) inflammation is the most crucial pathological event in asthma. In terms of whether T2 inflammation is dominant or not, asthma can be classified into T2-high and T2-low asthma. Currently, there exists a significant gap in our understanding of the heterogeneity of treatment-naive T2-high asthma patients. Moreover, no studies have examined the impacts of inhaled corticosteroids (ICS) on the airway microenvironment and metabolism of T2-high asthma during the early stage of treatment. This study, by employing multi-omic techniques, investigated the pathophysiological features and heterogeneity of untreated T2-high asthma, as well as the effects of ICS treatment. This study provided more in-depth insights into the pathophysiological mechanisms underlying T2-high asthma heterogeneity.
METHODS: Thirty-one treatment-naive T2-high asthma patients and fourteen healthy individuals were enrolled in this study. On the basis of hierarchical clustering analysis of T2 inflammation markers, fractional exhaled nitric oxide (FeNO) level and blood eosinophil count (BEC), the T2-high asthma patients were divided into three subgroups in terms of FeNO levels (≤ 25 ppb, 26-50 ppb, and > 50 ppb). All asthma patients underwent asthma control scoring, pulmonary function tests, and FeNO measurement at baseline and during a regular 3-month follow-up. Induced sputum and plasma were collected. Other tests included 16S rRNA microbiome profiling of the induced sputum, Luminex xMAP immunoassays of cytokines, and plasma metabolomic analysis using Q-Exactive liquid chromatography-mass spectrometry (LC-MS/MS). Meanwhile, data from the healthy population were also harvested.
RESULTS: T2-high asthma patients differed significantly from healthy controls in terms of airway inflammatory cytokines, airway microbial community structure, and plasma metabolic profiles. At baseline, T2-high asthma patients with different FeNO levels exhibited remarkable similarities in clinical symptoms, pulmonary function indices, airway cytokines, airway microbial diversity, and metabolites. After treatment with ICS, symptoms improved in T2-high asthma patients. The levels of FeNO, blood eosinophils, and total immunoglobulin E (tIgE) decreased significantly, while pulmonary function did not show substantial improvement. Some indices of airway cytokines underwent changes. No differences were found in airway microbial diversity; however, the abundance of Actinomyces increased. Moreover, the levels of glycerophospholipids and arachidonic acid metabolites decreased. Differentially expressed metabolites were enriched in arachidonic acid metabolism. The effect of ICS treatment varied among different T2-high asthma subgroups.
CONCLUSIONS: The airway local microenvironment and systemic metabolic profiles of treatment-naive T2-high asthma patients were distinctly different from those of healthy individuals. Limited heterogeneity was observed among patients stratified in terms of T2-inflammatory burden. ICS altered the airway microenvironment and rectified the lipid/arachidonic acid metabolic dysregulation. However, ICS effects varied across various T2-high subgroups.
Additional Links: PMID-41727967
PubMed:
Citation:
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@article {pmid41727967,
year = {2026},
author = {Duan, Y and Gu, Z and Liu, T and Song, C and Wang, Y and Wang, W and Jin, R and Wang, X and Zhang, Y and Huang, K},
title = {Effects of T2-high asthma heterogeneity and inhaled corticosteroid on airway and metabolic profiles: A multi-omic approach.},
journal = {Journal of translational internal medicine},
volume = {14},
number = {1},
pages = {79-95},
pmid = {41727967},
issn = {2450-131X},
abstract = {BACKGROUND AND OBJECTIVES: Asthma represents a heterogeneous chronic respiratory condition. Type 2 (T2) inflammation is the most crucial pathological event in asthma. In terms of whether T2 inflammation is dominant or not, asthma can be classified into T2-high and T2-low asthma. Currently, there exists a significant gap in our understanding of the heterogeneity of treatment-naive T2-high asthma patients. Moreover, no studies have examined the impacts of inhaled corticosteroids (ICS) on the airway microenvironment and metabolism of T2-high asthma during the early stage of treatment. This study, by employing multi-omic techniques, investigated the pathophysiological features and heterogeneity of untreated T2-high asthma, as well as the effects of ICS treatment. This study provided more in-depth insights into the pathophysiological mechanisms underlying T2-high asthma heterogeneity.
METHODS: Thirty-one treatment-naive T2-high asthma patients and fourteen healthy individuals were enrolled in this study. On the basis of hierarchical clustering analysis of T2 inflammation markers, fractional exhaled nitric oxide (FeNO) level and blood eosinophil count (BEC), the T2-high asthma patients were divided into three subgroups in terms of FeNO levels (≤ 25 ppb, 26-50 ppb, and > 50 ppb). All asthma patients underwent asthma control scoring, pulmonary function tests, and FeNO measurement at baseline and during a regular 3-month follow-up. Induced sputum and plasma were collected. Other tests included 16S rRNA microbiome profiling of the induced sputum, Luminex xMAP immunoassays of cytokines, and plasma metabolomic analysis using Q-Exactive liquid chromatography-mass spectrometry (LC-MS/MS). Meanwhile, data from the healthy population were also harvested.
RESULTS: T2-high asthma patients differed significantly from healthy controls in terms of airway inflammatory cytokines, airway microbial community structure, and plasma metabolic profiles. At baseline, T2-high asthma patients with different FeNO levels exhibited remarkable similarities in clinical symptoms, pulmonary function indices, airway cytokines, airway microbial diversity, and metabolites. After treatment with ICS, symptoms improved in T2-high asthma patients. The levels of FeNO, blood eosinophils, and total immunoglobulin E (tIgE) decreased significantly, while pulmonary function did not show substantial improvement. Some indices of airway cytokines underwent changes. No differences were found in airway microbial diversity; however, the abundance of Actinomyces increased. Moreover, the levels of glycerophospholipids and arachidonic acid metabolites decreased. Differentially expressed metabolites were enriched in arachidonic acid metabolism. The effect of ICS treatment varied among different T2-high asthma subgroups.
CONCLUSIONS: The airway local microenvironment and systemic metabolic profiles of treatment-naive T2-high asthma patients were distinctly different from those of healthy individuals. Limited heterogeneity was observed among patients stratified in terms of T2-inflammatory burden. ICS altered the airway microenvironment and rectified the lipid/arachidonic acid metabolic dysregulation. However, ICS effects varied across various T2-high subgroups.},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
BMI-stratified phenotypes of polycystic ovary syndrome: advances in gut microbiota research and personalized management strategies.
Frontiers in endocrinology, 17:1734041.
Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine-metabolic disorder affecting 11%-13% of women of reproductive age. Based on body mass index (BMI), patients can be phenotypically classified into obese and non-obese subgroups: the obese PCOS is characterized by insulin resistance, hyperandrogenemia, and metabolic syndrome, with more pronounced metabolic risks; non-obese PCOS primarily manifests as reproductive endocrine dysfunction. In recent years, studies have shown that the Gut microbiota plays a key role in the pathogenesis of PCOS, and dysbiosis in the obese subgroup is generally more pronounced, potentially amplifying metabolic abnormalities through pathways such as short-chain fatty acids, bile acid disturbances, and endotoxin-related low-grade inflammation. This review systematically summarizes the clinically heterogeneous features of BMI-stratified PCOS and its gut microbiota characteristics, with a focus on elucidating the mechanistic differences between obese and non-obese individuals in terms of inflammation, metabolites, and endocrine regulatory pathways. Based on current evidence, individualized intervention strategies targeting different BMI subtypes are proposed, including dietary and lifestyle modifications, interventions with probiotics/prebiotics/synbiotics, and exploration of emerging precision microbiome therapies such as fecal microbiota transplantation. The interaction between BMI and gut microbiota provides new directions for stratified management and personalized treatment of PCOS; however, high-quality longitudinal and interventional studies are still needed to clarify causal relationships and optimize microbiota-targeted strategies.
Additional Links: PMID-41727680
PubMed:
Citation:
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@article {pmid41727680,
year = {2026},
author = {Su, B and Cao, Y and Ma, L and Huang, J},
title = {BMI-stratified phenotypes of polycystic ovary syndrome: advances in gut microbiota research and personalized management strategies.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1734041},
pmid = {41727680},
issn = {1664-2392},
mesh = {Humans ; *Polycystic Ovary Syndrome/microbiology/therapy/pathology ; *Gastrointestinal Microbiome/physiology ; Female ; *Body Mass Index ; *Precision Medicine/methods ; *Obesity/complications/microbiology ; Phenotype ; Dysbiosis ; },
abstract = {Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine-metabolic disorder affecting 11%-13% of women of reproductive age. Based on body mass index (BMI), patients can be phenotypically classified into obese and non-obese subgroups: the obese PCOS is characterized by insulin resistance, hyperandrogenemia, and metabolic syndrome, with more pronounced metabolic risks; non-obese PCOS primarily manifests as reproductive endocrine dysfunction. In recent years, studies have shown that the Gut microbiota plays a key role in the pathogenesis of PCOS, and dysbiosis in the obese subgroup is generally more pronounced, potentially amplifying metabolic abnormalities through pathways such as short-chain fatty acids, bile acid disturbances, and endotoxin-related low-grade inflammation. This review systematically summarizes the clinically heterogeneous features of BMI-stratified PCOS and its gut microbiota characteristics, with a focus on elucidating the mechanistic differences between obese and non-obese individuals in terms of inflammation, metabolites, and endocrine regulatory pathways. Based on current evidence, individualized intervention strategies targeting different BMI subtypes are proposed, including dietary and lifestyle modifications, interventions with probiotics/prebiotics/synbiotics, and exploration of emerging precision microbiome therapies such as fecal microbiota transplantation. The interaction between BMI and gut microbiota provides new directions for stratified management and personalized treatment of PCOS; however, high-quality longitudinal and interventional studies are still needed to clarify causal relationships and optimize microbiota-targeted strategies.},
}
MeSH Terms:
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Humans
*Polycystic Ovary Syndrome/microbiology/therapy/pathology
*Gastrointestinal Microbiome/physiology
Female
*Body Mass Index
*Precision Medicine/methods
*Obesity/complications/microbiology
Phenotype
Dysbiosis
RevDate: 2026-02-23
CmpDate: 2026-02-23
Antimicrobial Resistance: The Answers.
British journal of biomedical science, 83:15559.
Antimicrobial resistance (AMR) has caused a global public health crisis, contributing to approximately five million deaths in 2019 and predicted deaths of approximately ten million annually by 2050. This equates to approximately 1.4-fold more deaths annually from AMR in 2050 than the entire COVID-19 pandemic to date. To tackle this AMR pandemic, regulatory and policy frameworks have been prepared at local, national and international levels with multi-faceted proposals and advances encompassing surveillance, diagnostics, infection prevention, antibiotic prescribing and variation of existing and novel treatment approaches. This narrative review primarily focuses on research and development which have been documented over the last five years in relation to therapeutic approaches at various stages in clinical development and the potential role that vaccines can play in the fight against AMR. This review provides an overview on antibacterial drugs, including novel classes of antibiotics, which have been recently approved, as well as combination antibiotic therapy and the potential of repurposed drugs. The potential role of novel antimicrobial, antibiofilm and quorum sensing inhibitors, such as antimicrobial peptides, nanomaterials and compounds from the extreme and natural environments, as well as ethnopharmacology including the antimicrobial effects of plants, spices, honey and venoms are explored. Novel therapeutic approaches are critically discussed in terms of their realistic clinical potential, detailing recent and ongoing trials to highlight the current interest of these approaches, including immunotherapy, bacteriophage therapy, antimicrobial photodynamic therapy (aPDT), antimicrobial sonodynamic therapy (aSDT), nitric oxide therapy and microbiome manipulation including faecal microbiota transplantation (FMT). The potential of predatory bacteria as living antimicrobial agents is also discussed. Importantly, there have been many technological developments which have enhanced bioprospecting and research and development of novel antimicrobials which this review draws attention to, including artificial intelligence, machine learning and Organ-on-a-Chip devices. Finally, key messages from the recent World Health Organization report into the role of vaccines against AMR provides an interesting perspective relating to prevention which can be of significance in tackling the AMR burden.
Additional Links: PMID-41727556
PubMed:
Citation:
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@article {pmid41727556,
year = {2026},
author = {Millar, BC and Cates, MJ and Torrisi, MS and Round, AJ and Warde, A and Lowery, CJ and Moore, JE},
title = {Antimicrobial Resistance: The Answers.},
journal = {British journal of biomedical science},
volume = {83},
number = {},
pages = {15559},
pmid = {41727556},
issn = {2474-0896},
mesh = {Humans ; *Anti-Bacterial Agents/therapeutic use/pharmacology ; *Drug Resistance, Bacterial ; COVID-19/epidemiology ; SARS-CoV-2 ; },
abstract = {Antimicrobial resistance (AMR) has caused a global public health crisis, contributing to approximately five million deaths in 2019 and predicted deaths of approximately ten million annually by 2050. This equates to approximately 1.4-fold more deaths annually from AMR in 2050 than the entire COVID-19 pandemic to date. To tackle this AMR pandemic, regulatory and policy frameworks have been prepared at local, national and international levels with multi-faceted proposals and advances encompassing surveillance, diagnostics, infection prevention, antibiotic prescribing and variation of existing and novel treatment approaches. This narrative review primarily focuses on research and development which have been documented over the last five years in relation to therapeutic approaches at various stages in clinical development and the potential role that vaccines can play in the fight against AMR. This review provides an overview on antibacterial drugs, including novel classes of antibiotics, which have been recently approved, as well as combination antibiotic therapy and the potential of repurposed drugs. The potential role of novel antimicrobial, antibiofilm and quorum sensing inhibitors, such as antimicrobial peptides, nanomaterials and compounds from the extreme and natural environments, as well as ethnopharmacology including the antimicrobial effects of plants, spices, honey and venoms are explored. Novel therapeutic approaches are critically discussed in terms of their realistic clinical potential, detailing recent and ongoing trials to highlight the current interest of these approaches, including immunotherapy, bacteriophage therapy, antimicrobial photodynamic therapy (aPDT), antimicrobial sonodynamic therapy (aSDT), nitric oxide therapy and microbiome manipulation including faecal microbiota transplantation (FMT). The potential of predatory bacteria as living antimicrobial agents is also discussed. Importantly, there have been many technological developments which have enhanced bioprospecting and research and development of novel antimicrobials which this review draws attention to, including artificial intelligence, machine learning and Organ-on-a-Chip devices. Finally, key messages from the recent World Health Organization report into the role of vaccines against AMR provides an interesting perspective relating to prevention which can be of significance in tackling the AMR burden.},
}
MeSH Terms:
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Humans
*Anti-Bacterial Agents/therapeutic use/pharmacology
*Drug Resistance, Bacterial
COVID-19/epidemiology
SARS-CoV-2
RevDate: 2026-02-23
CmpDate: 2026-02-23
Characterizing the Bacterial Microbiome of the Invasive Vector Aedes albopictus in Hungary: A Pilot Study Using Oxford Nanopore Sequencing.
International journal of microbiology, 2026:1956331.
Aedes albopictus has recently established self-sustaining populations in Hungary, but its microbiota-which may influence vector competence-remains poorly understood. We used Oxford Nanopore long-read sequencing for full-length 16S rRNA gene profiling of adult Ae. albopictus from two urban sites, Pécs and Barcs. Each location contributed 10 specimens, with contamination controls rigorously applied. Diversity metrics and co-occurrence network analyses were performed using QIIME2, SparCC, and NetCoMi, with robustness assessed via simulated node removal and addition. Sequencing depth was sufficient to saturate rarefaction curves. Although alpha and beta diversity did not differ significantly between sites, the Pécs population exhibited greater taxonomic richness (100 unique taxa vs. 61 in Barcs) and denser, more clustered networks. Only 15 genera were shared, with Wolbachia dominating both communities. Networks differed in central taxa and structural properties: Pécs retained higher connectivity and shorter paths under perturbation, suggesting greater resilience. Removal of conserved taxa revealed location-specific impacts on network stability, with Pécs more vulnerable to the loss of key genera. Negative interactions and compensatory taxa emerged post-removal, indicating distinct reconfiguration strategies. Our findings highlight marked local variation in microbiome structure and robustness, even across a 65-km gradient. These results establish a high-resolution baseline for assessing how microbiota shape Ae. albopictus vector potential, informing microbiome-based control strategies tailored to regional contexts.
Additional Links: PMID-41727526
PubMed:
Citation:
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@article {pmid41727526,
year = {2026},
author = {Kurucz, K and Philippe, C and Ábrahám, Á and Kratou, M and Piloto-Sardiñas, E and Obregon, D and Abuin-Denis, L and Kovács-Valasek, A and Cabezas-Cruz, A},
title = {Characterizing the Bacterial Microbiome of the Invasive Vector Aedes albopictus in Hungary: A Pilot Study Using Oxford Nanopore Sequencing.},
journal = {International journal of microbiology},
volume = {2026},
number = {},
pages = {1956331},
pmid = {41727526},
issn = {1687-918X},
abstract = {Aedes albopictus has recently established self-sustaining populations in Hungary, but its microbiota-which may influence vector competence-remains poorly understood. We used Oxford Nanopore long-read sequencing for full-length 16S rRNA gene profiling of adult Ae. albopictus from two urban sites, Pécs and Barcs. Each location contributed 10 specimens, with contamination controls rigorously applied. Diversity metrics and co-occurrence network analyses were performed using QIIME2, SparCC, and NetCoMi, with robustness assessed via simulated node removal and addition. Sequencing depth was sufficient to saturate rarefaction curves. Although alpha and beta diversity did not differ significantly between sites, the Pécs population exhibited greater taxonomic richness (100 unique taxa vs. 61 in Barcs) and denser, more clustered networks. Only 15 genera were shared, with Wolbachia dominating both communities. Networks differed in central taxa and structural properties: Pécs retained higher connectivity and shorter paths under perturbation, suggesting greater resilience. Removal of conserved taxa revealed location-specific impacts on network stability, with Pécs more vulnerable to the loss of key genera. Negative interactions and compensatory taxa emerged post-removal, indicating distinct reconfiguration strategies. Our findings highlight marked local variation in microbiome structure and robustness, even across a 65-km gradient. These results establish a high-resolution baseline for assessing how microbiota shape Ae. albopictus vector potential, informing microbiome-based control strategies tailored to regional contexts.},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
The microbial peace-signal hypothesis: distributed immune "peace hubs" across the human body.
Frontiers in immunology, 17:1738273.
The human immune system depends on microbial partners to maintain restraint. Short-chain fatty acids (SCFAs), produced by anaerobic fermenters in the gut, mouth, and skin, act as biochemical "peace signals" that calm immune activation and promote tolerance. In this hypothesis, "peace signals" refer primarily to microbially derived SCFAs; additional microbial metabolites are discussed as possible but more speculative contributors to immune restraint. This Microbial Peace-Signal Hypothesis proposes that immune homeostasis is not a static legacy of early-life microbial exposure, but a continuous partnership with these commensal fermenters. Modern lifestyle factors-including excessive hygiene, antibiotics, and low-fiber diets-have collapsed the ecological niches that support SCFA-producing guilds. Their loss silences microbial peace signals and drives the epidemic rise of allergies and autoimmune diseases. Unlike the "hygiene" or "old friends" hypotheses, this framework positions microbial peacekeeping as a lifelong metabolic function. It predicts that restoring SCFA producers across all major surfaces-gut, oral, and skin-will reduce immune overactivation systemically. This hypothesis unites clinical, ecological, and evolutionary evidence, suggesting that maintaining distributed SCFA-producing microbiomes is the foundation of long-term immune peace.
Additional Links: PMID-41727500
PubMed:
Citation:
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@article {pmid41727500,
year = {2026},
author = {Han, CS},
title = {The microbial peace-signal hypothesis: distributed immune "peace hubs" across the human body.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1738273},
pmid = {41727500},
issn = {1664-3224},
mesh = {Humans ; *Fatty Acids, Volatile/metabolism/immunology ; *Gastrointestinal Microbiome/immunology ; *Microbiota/immunology ; *Immune System/immunology ; Skin/immunology/microbiology ; Homeostasis/immunology ; Animals ; Hypersensitivity/immunology ; },
abstract = {The human immune system depends on microbial partners to maintain restraint. Short-chain fatty acids (SCFAs), produced by anaerobic fermenters in the gut, mouth, and skin, act as biochemical "peace signals" that calm immune activation and promote tolerance. In this hypothesis, "peace signals" refer primarily to microbially derived SCFAs; additional microbial metabolites are discussed as possible but more speculative contributors to immune restraint. This Microbial Peace-Signal Hypothesis proposes that immune homeostasis is not a static legacy of early-life microbial exposure, but a continuous partnership with these commensal fermenters. Modern lifestyle factors-including excessive hygiene, antibiotics, and low-fiber diets-have collapsed the ecological niches that support SCFA-producing guilds. Their loss silences microbial peace signals and drives the epidemic rise of allergies and autoimmune diseases. Unlike the "hygiene" or "old friends" hypotheses, this framework positions microbial peacekeeping as a lifelong metabolic function. It predicts that restoring SCFA producers across all major surfaces-gut, oral, and skin-will reduce immune overactivation systemically. This hypothesis unites clinical, ecological, and evolutionary evidence, suggesting that maintaining distributed SCFA-producing microbiomes is the foundation of long-term immune peace.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Fatty Acids, Volatile/metabolism/immunology
*Gastrointestinal Microbiome/immunology
*Microbiota/immunology
*Immune System/immunology
Skin/immunology/microbiology
Homeostasis/immunology
Animals
Hypersensitivity/immunology
RevDate: 2026-02-23
CmpDate: 2026-02-23
Pleiotropic immunoregulation by bile acids in pathophysiology.
Frontiers in immunology, 17:1719092.
Bile acids (BAs) have evolved from their classical role in lipid digestion to become central signaling molecules that integrate host metabolism, gut microbiota, and immune function. This review examines how diverse BAs regulate both innate and adaptive immunity through specific receptors-including farnesoid X receptor, Takeda G-protein-coupled receptor 5, vitamin D receptor, and retinoid orphan receptors-modulating the activity of macrophages, dendritic cells, T cells, natural killer cells, and natural killer T cells. Tissue-specific BA signaling influences immune homeostasis in the intestine, liver, central nervous system, and tumor microenvironment. Furthermore, we discuss the pathogenic role of dysregulated BA signaling in inflammatory, autoimmune, metabolic, and malignant diseases, and evaluate emerging therapeutic strategies that target BA pathways via synthetic ligands, engineered microbes, and dietary modulation. Leveraging BA-immune crosstalk to advance research on precision immunotherapy and microbiome-based interventions is a promising area of research.
Additional Links: PMID-41727485
PubMed:
Citation:
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@article {pmid41727485,
year = {2026},
author = {Lin, BS and Yin, MY and Xie, SA and Li, P and Li, X},
title = {Pleiotropic immunoregulation by bile acids in pathophysiology.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1719092},
pmid = {41727485},
issn = {1664-3224},
mesh = {Humans ; Animals ; *Bile Acids and Salts/metabolism/immunology ; Signal Transduction/immunology ; Adaptive Immunity ; Immunity, Innate ; *Immunomodulation ; Gastrointestinal Microbiome/immunology ; },
abstract = {Bile acids (BAs) have evolved from their classical role in lipid digestion to become central signaling molecules that integrate host metabolism, gut microbiota, and immune function. This review examines how diverse BAs regulate both innate and adaptive immunity through specific receptors-including farnesoid X receptor, Takeda G-protein-coupled receptor 5, vitamin D receptor, and retinoid orphan receptors-modulating the activity of macrophages, dendritic cells, T cells, natural killer cells, and natural killer T cells. Tissue-specific BA signaling influences immune homeostasis in the intestine, liver, central nervous system, and tumor microenvironment. Furthermore, we discuss the pathogenic role of dysregulated BA signaling in inflammatory, autoimmune, metabolic, and malignant diseases, and evaluate emerging therapeutic strategies that target BA pathways via synthetic ligands, engineered microbes, and dietary modulation. Leveraging BA-immune crosstalk to advance research on precision immunotherapy and microbiome-based interventions is a promising area of research.},
}
MeSH Terms:
show MeSH Terms
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Humans
Animals
*Bile Acids and Salts/metabolism/immunology
Signal Transduction/immunology
Adaptive Immunity
Immunity, Innate
*Immunomodulation
Gastrointestinal Microbiome/immunology
RevDate: 2026-02-23
CmpDate: 2026-02-23
Immunomodulatory effects of oral microbiota in the pathogenesis of rheumatoid arthritis.
Frontiers in immunology, 17:1707949.
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent synovial inflammation, progressive cartilage and bone destruction, and resulting functional disability. Its pathogenesis is multifactorial, involving both genetic predisposition and environmental influences. In recent years, the interaction between the oral microbiota and RA has emerged as a prominent research focus. Dysbiosis of the oral microbiome, defined as an imbalance in microbial composition relative to a healthy state, accompanies disease onset and may further act as a trigger of systemic autoimmune responses. Specific virulence factors, including the peptidylarginine deiminase from Porphyromonas gingivalis and leukotoxin A from Aggregatibacter actinomycetemcomitans, promote excessive protein citrullination and anti-citrullinated protein antibody generation, thereby contributing to the loss of immune tolerance, particularly in genetically susceptible individuals. Moreover, the bidirectional relationship between RA and periodontitis highlights shared inflammatory pathways that contribute to both periodontal and joint tissue destruction. Potential mechanisms include bacteremia induced by routine oral activities, systemic dissemination of bacterial products, and colonization of oral microbiota in the gastrointestinal tract. Current evidence suggests that periodontal therapy may reduce systemic inflammatory markers and occasionally improve RA activity, although results remain inconsistent. In this review, we explored the potential mechanisms underlying the imbalance of the oral microbiota and its contribution to the onset and progression of RA, focusing on microbially induced citrullination, host genetic susceptibility, and common inflammatory pathways, while also discussing the impact of comprehensive periodontal management and lifestyle interventions on RA outcomes. Overall, these insights underscore the role of the oral microbiome in RA pathogenesis and suggest that addressing microbial dysbiosis through integrated therapeutic strategies may complement conventional care.
Additional Links: PMID-41727451
PubMed:
Citation:
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@article {pmid41727451,
year = {2026},
author = {Yang, Y and Wang, G and Song, Y and Ma, J and Liu, A},
title = {Immunomodulatory effects of oral microbiota in the pathogenesis of rheumatoid arthritis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1707949},
pmid = {41727451},
issn = {1664-3224},
mesh = {Humans ; *Arthritis, Rheumatoid/immunology/microbiology/etiology/therapy ; *Mouth/microbiology/immunology ; *Microbiota/immunology ; Dysbiosis/immunology ; Animals ; *Immunomodulation ; Periodontitis/immunology/microbiology ; },
abstract = {Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent synovial inflammation, progressive cartilage and bone destruction, and resulting functional disability. Its pathogenesis is multifactorial, involving both genetic predisposition and environmental influences. In recent years, the interaction between the oral microbiota and RA has emerged as a prominent research focus. Dysbiosis of the oral microbiome, defined as an imbalance in microbial composition relative to a healthy state, accompanies disease onset and may further act as a trigger of systemic autoimmune responses. Specific virulence factors, including the peptidylarginine deiminase from Porphyromonas gingivalis and leukotoxin A from Aggregatibacter actinomycetemcomitans, promote excessive protein citrullination and anti-citrullinated protein antibody generation, thereby contributing to the loss of immune tolerance, particularly in genetically susceptible individuals. Moreover, the bidirectional relationship between RA and periodontitis highlights shared inflammatory pathways that contribute to both periodontal and joint tissue destruction. Potential mechanisms include bacteremia induced by routine oral activities, systemic dissemination of bacterial products, and colonization of oral microbiota in the gastrointestinal tract. Current evidence suggests that periodontal therapy may reduce systemic inflammatory markers and occasionally improve RA activity, although results remain inconsistent. In this review, we explored the potential mechanisms underlying the imbalance of the oral microbiota and its contribution to the onset and progression of RA, focusing on microbially induced citrullination, host genetic susceptibility, and common inflammatory pathways, while also discussing the impact of comprehensive periodontal management and lifestyle interventions on RA outcomes. Overall, these insights underscore the role of the oral microbiome in RA pathogenesis and suggest that addressing microbial dysbiosis through integrated therapeutic strategies may complement conventional care.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Arthritis, Rheumatoid/immunology/microbiology/etiology/therapy
*Mouth/microbiology/immunology
*Microbiota/immunology
Dysbiosis/immunology
Animals
*Immunomodulation
Periodontitis/immunology/microbiology
RevDate: 2026-02-23
CmpDate: 2026-02-23
Alterations in gut microbiota and plasma metabolites in pulmonary arterial hypertension secondary to congenital left-to-right shunt heart disease: potential mechanisms and biomarkers.
Frontiers in genetics, 17:1699787.
INTRODUCTION: Pulmonary arterial hypertension (PAH) secondary to congenital left-to-right shunt heart disease (CL-RSHD) is a life-threatening complication with unclear microbial and metabolic mechanisms. This study investigated gut microbiota and plasma metabolic alterations in CL-RSHD-associated PAH to identify biomarkers and mechanistic pathways.
METHODS: This cross-sectional study included 86 participants: healthy controls (HC, n = 13), CL-RSHD (n = 46), and CL-RSHD + PAH (n = 27). Gut microbiota was analyzed using 16S rRNA gene sequencing of the V3-V4 region on 41 fecal samples (HC, n = 9; CL-RSHD, n = 15; and CL-RSHD + PAH, n = 17). Untargeted plasma metabolomics was analyzed on all 86 plasma samples. Microbial diversity, differential taxa (DESeq2), metabolic pathways (OPLS-DA, KEGG), and biomarker potential (ROC curves) were assessed. Dynamic correlations linked microbiota-metabolite interactions.
RESULTS: CL-RSHD + PAH patients showed preserved α/β-diversity but distinct taxonomic shifts: enriched Lachnoclostridium phocaeense (Firmicutes) and reduced SCFA-producing Anaerostipes. Metabolomics revealed dysregulated steroid biosynthesis, cortisol metabolism, and oxidative stress pathways. Key metabolites, including elevated 5-hydroxymethylcytidine (5-hmC) and γ-L-glutamyl-L-cysteine, and reduced histidine intermediate D-E1IG3P, correlated with PAH severity. Strong microbiota-metabolite interactions (e.g., Lactonifactor-D-E1IG3P, r = 0.82, P < 0.01) suggested a disrupted vascular remodeling axis. Metabolites like ADP-glucose (AUC = 0.94) and 3-phenylpropyl glucosinolate (AUC = 0.92) showed high diagnostic accuracy.
CONCLUSION: CL-RSHD-associated PAH involves gut microbial restructuring and metabolic reprogramming linked to immune-inflammatory activation and oxidative stress. The Firmicutes-histidine metabolism axis emerges as a therapeutic target. Despite limitations, this study provides foundational insights into microbial-metabolic drivers of PAH, highlighting novel biomarkers for early diagnosis and intervention.
Additional Links: PMID-41727385
PubMed:
Citation:
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@article {pmid41727385,
year = {2026},
author = {Li, D and Zhao, T and Gong, X and Ahemaiti, Y and Wei, L and Huang, Y and Hu, S},
title = {Alterations in gut microbiota and plasma metabolites in pulmonary arterial hypertension secondary to congenital left-to-right shunt heart disease: potential mechanisms and biomarkers.},
journal = {Frontiers in genetics},
volume = {17},
number = {},
pages = {1699787},
pmid = {41727385},
issn = {1664-8021},
abstract = {INTRODUCTION: Pulmonary arterial hypertension (PAH) secondary to congenital left-to-right shunt heart disease (CL-RSHD) is a life-threatening complication with unclear microbial and metabolic mechanisms. This study investigated gut microbiota and plasma metabolic alterations in CL-RSHD-associated PAH to identify biomarkers and mechanistic pathways.
METHODS: This cross-sectional study included 86 participants: healthy controls (HC, n = 13), CL-RSHD (n = 46), and CL-RSHD + PAH (n = 27). Gut microbiota was analyzed using 16S rRNA gene sequencing of the V3-V4 region on 41 fecal samples (HC, n = 9; CL-RSHD, n = 15; and CL-RSHD + PAH, n = 17). Untargeted plasma metabolomics was analyzed on all 86 plasma samples. Microbial diversity, differential taxa (DESeq2), metabolic pathways (OPLS-DA, KEGG), and biomarker potential (ROC curves) were assessed. Dynamic correlations linked microbiota-metabolite interactions.
RESULTS: CL-RSHD + PAH patients showed preserved α/β-diversity but distinct taxonomic shifts: enriched Lachnoclostridium phocaeense (Firmicutes) and reduced SCFA-producing Anaerostipes. Metabolomics revealed dysregulated steroid biosynthesis, cortisol metabolism, and oxidative stress pathways. Key metabolites, including elevated 5-hydroxymethylcytidine (5-hmC) and γ-L-glutamyl-L-cysteine, and reduced histidine intermediate D-E1IG3P, correlated with PAH severity. Strong microbiota-metabolite interactions (e.g., Lactonifactor-D-E1IG3P, r = 0.82, P < 0.01) suggested a disrupted vascular remodeling axis. Metabolites like ADP-glucose (AUC = 0.94) and 3-phenylpropyl glucosinolate (AUC = 0.92) showed high diagnostic accuracy.
CONCLUSION: CL-RSHD-associated PAH involves gut microbial restructuring and metabolic reprogramming linked to immune-inflammatory activation and oxidative stress. The Firmicutes-histidine metabolism axis emerges as a therapeutic target. Despite limitations, this study provides foundational insights into microbial-metabolic drivers of PAH, highlighting novel biomarkers for early diagnosis and intervention.},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
Saccharomyces boulardii in patients with severe acute pancreatitis: a single center, open-label randomized controlled trial.
Burns & trauma, 14:tkag006.
BACKGROUND: Nosocomial infections in patients with severe acute pancreatitis (SAP) are frequently driven by impaired intestinal barrier function, which facilitates bacterial translocation and contributes to adverse clinical outcomes. Saccharomyces boulardii (S. boulardii) can reconstitute gut microbiota composition. We investigated whether S. boulardii combined with enteral nutrition (EN) affects the microbiome and nosocomial infections in SAP.
METHODS: This study is a single centre, open-label randomized controlled trial. We included 50 patients with SAP in a Chinese gastroenterology intensive care unit (ICU), randomized to Probiotic group (S. boulardii and EN) or the Control group (EN). Throat/oropharyngeal and rectal swabs were collected from patients with SAP on days 0, 1, 3, 6, 9, 12, and 15 of ICU admission. The primary endpoints were nosocomial infection and fungemia, whereas the secondary endpoints were ICU mortality, 28-day mortality, ICU stay, and length of hospital stay. All samples were subjected to full-length 16 s rRNA and internal transcribed spacer (ITS) sequencing. Multivariate analysis was performed using normalized microbial and corresponding clinical data.
RESULTS: After data processing, 213 16S rRNA and 120 ITS samples were analysed. S. boulardii prevented nosocomial infections (0/27 in the Probiotic group vs 5/23 in the Control group; P < 0.05). Intestinal fungi were closely associated with nosocomial infections. Bioinformatic analysis showed that S. boulardii prevented nosocomial infections by reducing intestinal bacterial perturbation and inhibiting the proliferation of Enterococcus in the intestine, and Candida in the respiratory tract and intestines.
CONCLUSIONS: S. boulardii in patients with SAP may positively alter the respiratory and intestinal microbiome and decrease the incidence of nosocomial infections.
TRIAL REGISTRATION: This study was approved by the Ethics Committee of Xinqiao Hospital, Army Medical University, Chongqing China (2021-yd030-01), which was retrospectively registered at the Chinese Clinical Trial Registry (ChiCTR2200056011, Date of Registration: 30/01/2022 https://www.chictr.org.cn/showproj.html?proj=151215).
Additional Links: PMID-41727357
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@article {pmid41727357,
year = {2026},
author = {He, JL and Ran, L and Xiao, X and Su, Y and Lin, H and Lu, C and Tang, B and Yang, S},
title = {Saccharomyces boulardii in patients with severe acute pancreatitis: a single center, open-label randomized controlled trial.},
journal = {Burns & trauma},
volume = {14},
number = {},
pages = {tkag006},
pmid = {41727357},
issn = {2321-3868},
abstract = {BACKGROUND: Nosocomial infections in patients with severe acute pancreatitis (SAP) are frequently driven by impaired intestinal barrier function, which facilitates bacterial translocation and contributes to adverse clinical outcomes. Saccharomyces boulardii (S. boulardii) can reconstitute gut microbiota composition. We investigated whether S. boulardii combined with enteral nutrition (EN) affects the microbiome and nosocomial infections in SAP.
METHODS: This study is a single centre, open-label randomized controlled trial. We included 50 patients with SAP in a Chinese gastroenterology intensive care unit (ICU), randomized to Probiotic group (S. boulardii and EN) or the Control group (EN). Throat/oropharyngeal and rectal swabs were collected from patients with SAP on days 0, 1, 3, 6, 9, 12, and 15 of ICU admission. The primary endpoints were nosocomial infection and fungemia, whereas the secondary endpoints were ICU mortality, 28-day mortality, ICU stay, and length of hospital stay. All samples were subjected to full-length 16 s rRNA and internal transcribed spacer (ITS) sequencing. Multivariate analysis was performed using normalized microbial and corresponding clinical data.
RESULTS: After data processing, 213 16S rRNA and 120 ITS samples were analysed. S. boulardii prevented nosocomial infections (0/27 in the Probiotic group vs 5/23 in the Control group; P < 0.05). Intestinal fungi were closely associated with nosocomial infections. Bioinformatic analysis showed that S. boulardii prevented nosocomial infections by reducing intestinal bacterial perturbation and inhibiting the proliferation of Enterococcus in the intestine, and Candida in the respiratory tract and intestines.
CONCLUSIONS: S. boulardii in patients with SAP may positively alter the respiratory and intestinal microbiome and decrease the incidence of nosocomial infections.
TRIAL REGISTRATION: This study was approved by the Ethics Committee of Xinqiao Hospital, Army Medical University, Chongqing China (2021-yd030-01), which was retrospectively registered at the Chinese Clinical Trial Registry (ChiCTR2200056011, Date of Registration: 30/01/2022 https://www.chictr.org.cn/showproj.html?proj=151215).},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
Latilactobacillus sakei strains protect crucian carp against Aeromonas hydrophila-induced intestinal injury in an oral challenge model.
Frontiers in nutrition, 13:1768111.
In aquaculture, the overuse of antibiotic could lead to antimicrobial resistance and destabilize host-microbiota homeostasis. Latilactobacillus sakei, belonging to the genus Latilactobacillus, was included in the list of bacteria that could be used in food in China in 2014. Increasing evidence demonstrated that its antagonistic capacity against a broad spectrum of pathogenic bacteria, indicating its promising potential for application in aquaculture. In this study, the protective effect of three L. sakei (JO12, JO26, JO35), isolated from the intestine of fish and shrimp, on mucosal injury caused by Aeromonas hydrophila in crucian carp under an oral challenge model was investigated. The result showed that compared with LGG, all three L. sakei strains alleviated A. hydrophila induced intestinal barrier damage and inflammation (downregulated intestinal TNF-α/IL-1β, upregulated IL-10, and reduced MyD88) in crucian carp. L. sakei JO35 delivered the greatest improvement in growth and feed efficiency. Compared with the model group, L. sakei JO26 and JO35 significantly decreased the levels of serum acid phosphatase (ACP) and increased intestinal lysozyme, whereas L. sakei JO12 lowerd serum ACP but exacerbated the elevation of intestinal AKP. Microbiome and transcriptome analysis revealed that the protective effect of L. sakei may be associated with the strain's intestinal colonization capacity and its regulation of phagolysosomal competence (lysosome/phagosome, LAMP) and IgA barrier via pIgR (prominent with JO35).
Additional Links: PMID-41727208
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@article {pmid41727208,
year = {2026},
author = {Zhao, Y and Li, R and Zhu, T and Hu, H and An, G and Ren, Z and Cui, J and Jiang, J},
title = {Latilactobacillus sakei strains protect crucian carp against Aeromonas hydrophila-induced intestinal injury in an oral challenge model.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1768111},
pmid = {41727208},
issn = {2296-861X},
abstract = {In aquaculture, the overuse of antibiotic could lead to antimicrobial resistance and destabilize host-microbiota homeostasis. Latilactobacillus sakei, belonging to the genus Latilactobacillus, was included in the list of bacteria that could be used in food in China in 2014. Increasing evidence demonstrated that its antagonistic capacity against a broad spectrum of pathogenic bacteria, indicating its promising potential for application in aquaculture. In this study, the protective effect of three L. sakei (JO12, JO26, JO35), isolated from the intestine of fish and shrimp, on mucosal injury caused by Aeromonas hydrophila in crucian carp under an oral challenge model was investigated. The result showed that compared with LGG, all three L. sakei strains alleviated A. hydrophila induced intestinal barrier damage and inflammation (downregulated intestinal TNF-α/IL-1β, upregulated IL-10, and reduced MyD88) in crucian carp. L. sakei JO35 delivered the greatest improvement in growth and feed efficiency. Compared with the model group, L. sakei JO26 and JO35 significantly decreased the levels of serum acid phosphatase (ACP) and increased intestinal lysozyme, whereas L. sakei JO12 lowerd serum ACP but exacerbated the elevation of intestinal AKP. Microbiome and transcriptome analysis revealed that the protective effect of L. sakei may be associated with the strain's intestinal colonization capacity and its regulation of phagolysosomal competence (lysosome/phagosome, LAMP) and IgA barrier via pIgR (prominent with JO35).},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
Better together: Microbial diversity might facilitate the invasion success of the seagrass Halophila stipulacea in mixed Mediterranean seagrass communities.
bioRxiv : the preprint server for biology pii:2026.02.09.704841.
Microorganisms are increasingly recognized as key facilitators of invasion success for introduced species into new environments. The globally invasive seagrass Halophila stipulacea flourishes in mixed environments with native seagrasses, where it exhibits enhanced growth, while, in contrast, native seagrasses in mixed environments experience reduced growth. Here, we hypothesize that microbes may support the success of invasive seagrass in mixed Mediterranean environments. We analyzed 16S rRNA genes to characterize the microbial diversity on the phyllosphere alongside biochemical, morphological, and sediment nutrient measurements of the Mediterranean-native seagrass Cymodocea nodosa and the invasive H. stipulacea from a controlled mesocosm experiment. Overall, C. nodosa in monoculture harbored a microbiome exhibiting higher ASV richness and a distinct community composition than H. stipulacea . Variation in bacterial diversity associated with hydrogen peroxide (H 2 O 2) and internode length suggests that microbial communities of the native seagrass might be shaped by its stress. Conversely, H. stipulacea's microbiome was most abundant in mixed environments, with bacteria significantly reduced in monoculture, and bacterial diversity loosely associated with growth, suggesting that microbes are critical to assisting and possibly facilitating H. stipulacea in mixed environments. Overall, our findings suggest that invasive H. stipulacea in the Mediterranean Sea are capable of recruiting beneficial bacteria, creating microbial interactions that support its success, and undermining the resilience of native seagrasses in mixed beds. Future work should center on the mechanisms driving H. stipulacea bacterial communities and investigating whether H. stipulacea actively determines its own microbiome, or whether its microbiome is passively determined by environmental variables.
Additional Links: PMID-41727154
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@article {pmid41727154,
year = {2026},
author = {Hoza-Frederick, E and Martínez-Campos, S and Barber, PH and Vasquez, MI and Fotopoulos, V and Antoniou, C and Drakou, K and Godoy-Vitorino, F and Chiquillo, KL},
title = {Better together: Microbial diversity might facilitate the invasion success of the seagrass Halophila stipulacea in mixed Mediterranean seagrass communities.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.02.09.704841},
pmid = {41727154},
issn = {2692-8205},
abstract = {Microorganisms are increasingly recognized as key facilitators of invasion success for introduced species into new environments. The globally invasive seagrass Halophila stipulacea flourishes in mixed environments with native seagrasses, where it exhibits enhanced growth, while, in contrast, native seagrasses in mixed environments experience reduced growth. Here, we hypothesize that microbes may support the success of invasive seagrass in mixed Mediterranean environments. We analyzed 16S rRNA genes to characterize the microbial diversity on the phyllosphere alongside biochemical, morphological, and sediment nutrient measurements of the Mediterranean-native seagrass Cymodocea nodosa and the invasive H. stipulacea from a controlled mesocosm experiment. Overall, C. nodosa in monoculture harbored a microbiome exhibiting higher ASV richness and a distinct community composition than H. stipulacea . Variation in bacterial diversity associated with hydrogen peroxide (H 2 O 2) and internode length suggests that microbial communities of the native seagrass might be shaped by its stress. Conversely, H. stipulacea's microbiome was most abundant in mixed environments, with bacteria significantly reduced in monoculture, and bacterial diversity loosely associated with growth, suggesting that microbes are critical to assisting and possibly facilitating H. stipulacea in mixed environments. Overall, our findings suggest that invasive H. stipulacea in the Mediterranean Sea are capable of recruiting beneficial bacteria, creating microbial interactions that support its success, and undermining the resilience of native seagrasses in mixed beds. Future work should center on the mechanisms driving H. stipulacea bacterial communities and investigating whether H. stipulacea actively determines its own microbiome, or whether its microbiome is passively determined by environmental variables.},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
Alamandine/MrgD Pathway Modulates Gut-Bone Marrow Axis in Aging.
bioRxiv : the preprint server for biology pii:2026.02.12.705187.
Aging is associated with colon epithelial barrier integrity and upregulation of myelopoiesis in the bone marrow (BM). Alamandine (Ala) and MrgD are novel members of the renin angiotensin system (RAS). This study tested the hypothesis that Ala restores the colon epithelial barrier integrity in aging via modulating gut-BM axis. Mice of age 2-3 (Young) or 22-24 months (Old) were treated with saline or Ala by using Osmotic pumps. The intestinal permeability was evaluated by using FITC-dextran. Lgr5 [+] Olfm4 [+] intestinal stem cells (ISCs), Wnt3a and β-catenin were evaluated by immunohistochemistry or western blotting. Fecal microbiome was analyzed by 16S rRNA sequencing. Monocyte-macrophages were characterized by flow cytometry. Cecal or serum bacterial metabolites were analyzed. The pro-myelopoietic potential of cecal supernatants (CS) was tested in the Young-BM cells. MrgD was expressed in ISCs, which was decreased in the Old. Increased intestinal permeability in aging was reversed by Ala. In the colon organoids, Ala increased Wnt3a levels that were antagonized by the NF449, SQ22536 or 666-15. Ala restored phospho-CREB and active β-catenin levels that were decreased in the Old colon-organoids. Ala increased the richness and β-diversity of the aging microbiome and decreased Bacillota / Bacteroidota . Ala decreased the CD80 [+] and increased CX3CR [+] cells in the Old colons. Old-CS induced myelopoiesis in vitro in BM cells with higher number of monocytes and pro-inflammatory macrophages which was not observed in the CS derived from Ala-treated Old mice. Ala is a promising pharmacological agent for reversing the leaky gut of aging by restoring homeostasis in the gut-BM axis.
Additional Links: PMID-41727025
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@article {pmid41727025,
year = {2026},
author = {Chittimalli, K and Rozario, HE and Martinez, V and McAdams, ZL and Adkins, SA and Ericsson, AC and Jarajapu, YP},
title = {Alamandine/MrgD Pathway Modulates Gut-Bone Marrow Axis in Aging.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.02.12.705187},
pmid = {41727025},
issn = {2692-8205},
abstract = {Aging is associated with colon epithelial barrier integrity and upregulation of myelopoiesis in the bone marrow (BM). Alamandine (Ala) and MrgD are novel members of the renin angiotensin system (RAS). This study tested the hypothesis that Ala restores the colon epithelial barrier integrity in aging via modulating gut-BM axis. Mice of age 2-3 (Young) or 22-24 months (Old) were treated with saline or Ala by using Osmotic pumps. The intestinal permeability was evaluated by using FITC-dextran. Lgr5 [+] Olfm4 [+] intestinal stem cells (ISCs), Wnt3a and β-catenin were evaluated by immunohistochemistry or western blotting. Fecal microbiome was analyzed by 16S rRNA sequencing. Monocyte-macrophages were characterized by flow cytometry. Cecal or serum bacterial metabolites were analyzed. The pro-myelopoietic potential of cecal supernatants (CS) was tested in the Young-BM cells. MrgD was expressed in ISCs, which was decreased in the Old. Increased intestinal permeability in aging was reversed by Ala. In the colon organoids, Ala increased Wnt3a levels that were antagonized by the NF449, SQ22536 or 666-15. Ala restored phospho-CREB and active β-catenin levels that were decreased in the Old colon-organoids. Ala increased the richness and β-diversity of the aging microbiome and decreased Bacillota / Bacteroidota . Ala decreased the CD80 [+] and increased CX3CR [+] cells in the Old colons. Old-CS induced myelopoiesis in vitro in BM cells with higher number of monocytes and pro-inflammatory macrophages which was not observed in the CS derived from Ala-treated Old mice. Ala is a promising pharmacological agent for reversing the leaky gut of aging by restoring homeostasis in the gut-BM axis.},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
Microbiome depletion rejuvenates the aging brain.
bioRxiv : the preprint server for biology pii:2026.02.13.705770.
Aging is associated with cognitive decline and increased vulnerability to neurodegeneration driven by an array of molecular and cellular changes like impaired vascular integrity, demyelination, reduced neurogenesis, and chronic inflammation. Recent studies implicate the gut microbiome as a modulator of brain aging, but the underlying mechanisms remain elusive. Here, we show that depleting the gut microbiome by administering antibiotics to aged mice induces widespread molecular and structural rejuvenation in the brain. Our transcriptomic analyses by single-nucleus RNA sequencing revealed pronounced transcriptional shifts across multiple brain cell types. We confirmed that antibiotic treatment improves vascular density, promotes myelination, enhances neurogenesis, and reduces microglial reactivity. Functionally, microbiome-depleted mice showed improved hippocampal memory performance. Analyses of brain and plasma cytokine levels showed a decrease in several pro-inflammatory factors post-treatment and identified candidate factors, including the chemokine eotaxin-1. Inhibiting eotaxin-1 alone can reverse several aspects of brain aging. Our findings demonstrate that age-associated microbial inflammation contributes to brain aging and that its attenuation can restore youthful features at the molecular, cellular, and functional levels. Targeting the gut microbiome or its circulating mediators may therefore represent a non-invasive approach to promote brain health and cognitive resilience in aging.
Additional Links: PMID-41727000
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@article {pmid41727000,
year = {2026},
author = {Gasperini, C and Holton, KM and Limone, F and Juttu, M and DeMeo, CC and Kekrtova, K and Patankar, S and Wells, KM and Giadone, RM and Driss, LB and Wei, G and Kiem, A and Xu, Q and Lee, RT and Friedlander, M and Scadden, DT and Rubin, LL},
title = {Microbiome depletion rejuvenates the aging brain.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.02.13.705770},
pmid = {41727000},
issn = {2692-8205},
abstract = {Aging is associated with cognitive decline and increased vulnerability to neurodegeneration driven by an array of molecular and cellular changes like impaired vascular integrity, demyelination, reduced neurogenesis, and chronic inflammation. Recent studies implicate the gut microbiome as a modulator of brain aging, but the underlying mechanisms remain elusive. Here, we show that depleting the gut microbiome by administering antibiotics to aged mice induces widespread molecular and structural rejuvenation in the brain. Our transcriptomic analyses by single-nucleus RNA sequencing revealed pronounced transcriptional shifts across multiple brain cell types. We confirmed that antibiotic treatment improves vascular density, promotes myelination, enhances neurogenesis, and reduces microglial reactivity. Functionally, microbiome-depleted mice showed improved hippocampal memory performance. Analyses of brain and plasma cytokine levels showed a decrease in several pro-inflammatory factors post-treatment and identified candidate factors, including the chemokine eotaxin-1. Inhibiting eotaxin-1 alone can reverse several aspects of brain aging. Our findings demonstrate that age-associated microbial inflammation contributes to brain aging and that its attenuation can restore youthful features at the molecular, cellular, and functional levels. Targeting the gut microbiome or its circulating mediators may therefore represent a non-invasive approach to promote brain health and cognitive resilience in aging.},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
Temporal dynamics of microbiome communities within urban compost piles undergoing the heat process.
bioRxiv : the preprint server for biology pii:2026.02.10.705224.
Urban composting supports soil health but also intersects with food safety, where compost is produced near farms and communities. Here, we profiled temporal microbiome dynamics across a 6-week heat compost cycle from the urban compost piles using paired physicochemical panels and long-read metagenomics. Nutrient composition and pH shifted with compost age, coinciding with stage-structured microbial succession, including temperature-linked turnover of compost communities from mesophilic to thermotolerant taxa. Bacterial profiles included the presence of antimicrobial resistance genes and foodborne-associated genera early in the cycle, with reduced representation during the thermophilic phase. Analysis of previously unclassified long reads reveals an extensive repertoire of putative bacteriophages, including several complete genomes and candidates linked to foodborne bacteria, and their abundance is coupled to the host abundance. Together, these results support thermophilic composting as a key mitigation step for microbiological hazards in urban-adjacent systems and identify compost piles as a promising reservoir for discovering candidate lytic phages for downstream isolation and host-range testing.
Additional Links: PMID-41726932
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@article {pmid41726932,
year = {2026},
author = {Montes, A and Klopmanbaerselman, D and Lee, B and Quiñones, B and Shim, H},
title = {Temporal dynamics of microbiome communities within urban compost piles undergoing the heat process.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.02.10.705224},
pmid = {41726932},
issn = {2692-8205},
abstract = {Urban composting supports soil health but also intersects with food safety, where compost is produced near farms and communities. Here, we profiled temporal microbiome dynamics across a 6-week heat compost cycle from the urban compost piles using paired physicochemical panels and long-read metagenomics. Nutrient composition and pH shifted with compost age, coinciding with stage-structured microbial succession, including temperature-linked turnover of compost communities from mesophilic to thermotolerant taxa. Bacterial profiles included the presence of antimicrobial resistance genes and foodborne-associated genera early in the cycle, with reduced representation during the thermophilic phase. Analysis of previously unclassified long reads reveals an extensive repertoire of putative bacteriophages, including several complete genomes and candidates linked to foodborne bacteria, and their abundance is coupled to the host abundance. Together, these results support thermophilic composting as a key mitigation step for microbiological hazards in urban-adjacent systems and identify compost piles as a promising reservoir for discovering candidate lytic phages for downstream isolation and host-range testing.},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
Functional Equivalence of Heat-Inactivated (HI) and Live Probiotic RSB11 in Suppressing Inflammation: Expanding Formulation and Application Potential.
bioRxiv : the preprint server for biology pii:2026.02.11.705228.
UNLABELLED: The clinical potential of probiotics has been widely recognized, but their translation into reliable therapeutic products has been hindered by major limitations such as undesirable immunogenic responses, the need to maintain viability, instability during storage and transport, and concerns regarding safety in vulnerable populations. Postbiotics, defined as inanimate microbial cells or their components with pro-health activities, overcome many of these limitations by offering enhanced stability, reproducibility, and safety. However, it is very vital to understand if the heat inactivation (conversion of a probiotic to its postbiotic inert form) compromise its functional efficacy. Here, we systematically compared a novel probiotic-derived candidate, Lactiplantibacillus plantarum RSB11 strain, in its live (RSB11 Life, probiotic) and heat-inactivated (RSB11-HI, postbiotic) forms across multiple human epithelial and non-epithelial models relevant to inflammation driven pathologies. To investigate the gut-tissue(s)-axis concept we used gut (Caco-2), lung (HBE), ovary (BG1), bone (osteoblasts, MG-63), kidney (A-498) and liver (HepG2) cells exposed to E-coli or lipopolysaccharide (LPS), and quantified matrix metalloproteinase-9 (MMP-9), an inflammatory mediator, by qPCR and pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), IL-6, and IL-1β by ELISA. In addition, we assessed β-glucuronidase activity and estrogen modulation to explore gut-ovarian axis signaling. Across all models, both RSB11 Life and RSB11-HI robustly suppressed MMP-9, TNF-α, IL-6 and IL-1β induction, with equivalent magnitude of effect. The inactivated form retained full cytokine-suppressive capacity and, notably, enhanced β-glucuronidase activity, suggesting additional benefits in microbiome hormone cross-talk. Our findings demonstrate that heat inactivation does not compromise, and may even expand, the functional range of RSB11. By maintaining bioactivity while eliminating the drawbacks of live biotics, heat inactivated RSB11 emerges as a robust, scalable, and versatile postbiotic with potential applications in systemic inflammatory disorders.
Heat-inactivated postbiotic RSB11-HI retains the anti-inflammatory efficacy of its live counterpart (RSB11Life) across diverse organ-relevant cell models. Upon LPS or E-coli stimulation, epithelial, immune, and tissue-specific cells (gut, lung, ovary, bone, kidney, liver) upregulate pro-inflammatory mediators including MMP-9, TNF-α, IL-6, and IL-1β. Both RSB11Life and RSB11-HI effectively suppress these inflammatory responses, with RSB11-HI exhibiting more consistent and robust reductions of inflammatory markers across models. Additionally, RSB11-HI uniquely enhances β-glucuronidase activity, facilitating estrogen metabolism and signaling through the gut-ovary axis. Together, these findings highlight RSB11-HI as a stable, safe, and multifunctional postbiotic candidate suitable for therapeutic formulation. Image was designed using ChatGPT .
Additional Links: PMID-41726906
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@article {pmid41726906,
year = {2026},
author = {Nicola, T and Madhvacharyula, T and Ashok, A and Mandot, A and Abdelgawad, I and Singh, R and Siedman, K and Yang, Y and Ambalavanan, N and Lal, CV},
title = {Functional Equivalence of Heat-Inactivated (HI) and Live Probiotic RSB11 in Suppressing Inflammation: Expanding Formulation and Application Potential.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.02.11.705228},
pmid = {41726906},
issn = {2692-8205},
abstract = {UNLABELLED: The clinical potential of probiotics has been widely recognized, but their translation into reliable therapeutic products has been hindered by major limitations such as undesirable immunogenic responses, the need to maintain viability, instability during storage and transport, and concerns regarding safety in vulnerable populations. Postbiotics, defined as inanimate microbial cells or their components with pro-health activities, overcome many of these limitations by offering enhanced stability, reproducibility, and safety. However, it is very vital to understand if the heat inactivation (conversion of a probiotic to its postbiotic inert form) compromise its functional efficacy. Here, we systematically compared a novel probiotic-derived candidate, Lactiplantibacillus plantarum RSB11 strain, in its live (RSB11 Life, probiotic) and heat-inactivated (RSB11-HI, postbiotic) forms across multiple human epithelial and non-epithelial models relevant to inflammation driven pathologies. To investigate the gut-tissue(s)-axis concept we used gut (Caco-2), lung (HBE), ovary (BG1), bone (osteoblasts, MG-63), kidney (A-498) and liver (HepG2) cells exposed to E-coli or lipopolysaccharide (LPS), and quantified matrix metalloproteinase-9 (MMP-9), an inflammatory mediator, by qPCR and pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), IL-6, and IL-1β by ELISA. In addition, we assessed β-glucuronidase activity and estrogen modulation to explore gut-ovarian axis signaling. Across all models, both RSB11 Life and RSB11-HI robustly suppressed MMP-9, TNF-α, IL-6 and IL-1β induction, with equivalent magnitude of effect. The inactivated form retained full cytokine-suppressive capacity and, notably, enhanced β-glucuronidase activity, suggesting additional benefits in microbiome hormone cross-talk. Our findings demonstrate that heat inactivation does not compromise, and may even expand, the functional range of RSB11. By maintaining bioactivity while eliminating the drawbacks of live biotics, heat inactivated RSB11 emerges as a robust, scalable, and versatile postbiotic with potential applications in systemic inflammatory disorders.
Heat-inactivated postbiotic RSB11-HI retains the anti-inflammatory efficacy of its live counterpart (RSB11Life) across diverse organ-relevant cell models. Upon LPS or E-coli stimulation, epithelial, immune, and tissue-specific cells (gut, lung, ovary, bone, kidney, liver) upregulate pro-inflammatory mediators including MMP-9, TNF-α, IL-6, and IL-1β. Both RSB11Life and RSB11-HI effectively suppress these inflammatory responses, with RSB11-HI exhibiting more consistent and robust reductions of inflammatory markers across models. Additionally, RSB11-HI uniquely enhances β-glucuronidase activity, facilitating estrogen metabolism and signaling through the gut-ovary axis. Together, these findings highlight RSB11-HI as a stable, safe, and multifunctional postbiotic candidate suitable for therapeutic formulation. Image was designed using ChatGPT .},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
The ketogenic diet alters microbiome-metabolome profiles to improve West syndrome therapy.
Pediatric investigation, 10(1):10-24.
IMPORTANCE: The ketogenic diet (KD) is effective in managing epilepsy, particularly West syndrome (WS); however, the role of gut microbiome (GM) and metabolome in its efficacy remains unclear. Understanding these mechanisms could optimize the KD for WS treatment.
OBJECTIVE: To identify microbiome-metabolome signatures associated with KD efficacy in WS by analyzing changes in GM composition and metabolic pathways.
METHODS: Fecal samples were collected from WS patients (n = 16) and healthy children (n = 24). Metagenome and metabolome analyses were performed to assess GM composition and metabolic profiles.
RESULTS: WS patients showed GM imbalances compared to healthy children. Disease status contributed sufficiently to the GM. The abundance of Bacteroides, Parabacteroides, and Faecalibacterium was lower in WS (3.30% vs. 39.86%, P-adj = 0.140; 0.14% vs. 0.73%, P-adj = 0.023; 0.04% vs. 1.35%, P-adj = 0.018), whereas Bifidobacterium and Escherichia were higher (6.08% vs. 2.23%, P-adj = 0.140; 7.57% vs. 0.15%, P-adj < 0.001). After KD, Parabacteroides (particularly P. distasonis) and Bacteroides (particularly B. fragilis) increased (0.14% vs. 0.35%, P-adj = 0.034; 3.30% vs. 21.18%, P-adj = 0.380); Bifidobacterium (particularly B. breve) and Escherichia (particularly E. coli) decreased from 6.08% and 7.57% to 1.24% and 2.52%, respectively. Kyoto Encyclopedia of Genes and Genomes pathway analysis demonstrated that ATP-binding cassette (ABC) transporters, fatty acid biosynthesis, tyrosine metabolism, and other pathways were significantly altered in patients with WS, and these alterations were reversed following ketogenic diet (KD) consumption. The KD also altered intestinal metabolites. Integrative analysis of microbial features, gene functions, and metabolites revealed that Bacteroides species and P. distasonis were significantly associated with ABC transporters, alanine aspartate and glutamate metabolism, and negatively correlated with 3-sulfinoalanine, suggesting potential regulatory roles in metabolic pathways.
INTERPRETATION: KD induces significant shifts in GM composition and metabolic pathways, which may contribute to its therapeutic efficacy in WS. The restoration of Bacteroides and Parabacteroides dominance, alongside alterations in gene functions and neurotransmitter-related metabolites, suggests a potential mechanism for the antiepileptic effects of KD.
Additional Links: PMID-41726584
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@article {pmid41726584,
year = {2026},
author = {Xie, G and Zhou, Q and Liao, J and Zheng, Y and Wang, W and Shen, K},
title = {The ketogenic diet alters microbiome-metabolome profiles to improve West syndrome therapy.},
journal = {Pediatric investigation},
volume = {10},
number = {1},
pages = {10-24},
pmid = {41726584},
issn = {2574-2272},
abstract = {IMPORTANCE: The ketogenic diet (KD) is effective in managing epilepsy, particularly West syndrome (WS); however, the role of gut microbiome (GM) and metabolome in its efficacy remains unclear. Understanding these mechanisms could optimize the KD for WS treatment.
OBJECTIVE: To identify microbiome-metabolome signatures associated with KD efficacy in WS by analyzing changes in GM composition and metabolic pathways.
METHODS: Fecal samples were collected from WS patients (n = 16) and healthy children (n = 24). Metagenome and metabolome analyses were performed to assess GM composition and metabolic profiles.
RESULTS: WS patients showed GM imbalances compared to healthy children. Disease status contributed sufficiently to the GM. The abundance of Bacteroides, Parabacteroides, and Faecalibacterium was lower in WS (3.30% vs. 39.86%, P-adj = 0.140; 0.14% vs. 0.73%, P-adj = 0.023; 0.04% vs. 1.35%, P-adj = 0.018), whereas Bifidobacterium and Escherichia were higher (6.08% vs. 2.23%, P-adj = 0.140; 7.57% vs. 0.15%, P-adj < 0.001). After KD, Parabacteroides (particularly P. distasonis) and Bacteroides (particularly B. fragilis) increased (0.14% vs. 0.35%, P-adj = 0.034; 3.30% vs. 21.18%, P-adj = 0.380); Bifidobacterium (particularly B. breve) and Escherichia (particularly E. coli) decreased from 6.08% and 7.57% to 1.24% and 2.52%, respectively. Kyoto Encyclopedia of Genes and Genomes pathway analysis demonstrated that ATP-binding cassette (ABC) transporters, fatty acid biosynthesis, tyrosine metabolism, and other pathways were significantly altered in patients with WS, and these alterations were reversed following ketogenic diet (KD) consumption. The KD also altered intestinal metabolites. Integrative analysis of microbial features, gene functions, and metabolites revealed that Bacteroides species and P. distasonis were significantly associated with ABC transporters, alanine aspartate and glutamate metabolism, and negatively correlated with 3-sulfinoalanine, suggesting potential regulatory roles in metabolic pathways.
INTERPRETATION: KD induces significant shifts in GM composition and metabolic pathways, which may contribute to its therapeutic efficacy in WS. The restoration of Bacteroides and Parabacteroides dominance, alongside alterations in gene functions and neurotransmitter-related metabolites, suggests a potential mechanism for the antiepileptic effects of KD.},
}
RevDate: 2026-02-24
CmpDate: 2026-02-23
Distinguishing the significance of blood microbes in epithelial ovarian cancer.
Gut microbes reports, 3(1):.
The human microbiome has generated growing interest in epithelial ovarian cancer (EOC) research, yet investigations of the blood microbiome remain sparse. This study explored plasma microbial signatures unique to EOC. We accessed 180 age/race/ethnicity-matched archival plasma samples from women with (1) EOC; (2) commonly diagnosed non-EOC solid tumors in women; (3) benign gynecologic conditions; and (4) age/race/ethnicity-matched controls. The microbial profiles of the plasma specimens were assessed using an amplicon-based sequencing method that targets the 16S rRNA gene in the bacterial genome. A stringent bioinformatic pipeline was applied to filter out suspicious bacterial contaminants at the genus level. Bioinformatic decontamination analysis removed 225 high-risk bacterial contaminants. The remaining 339 high-confidence bacteria were included in the final analysis for differential abundances in the plasma between the study groups. Women with EOC, which were primarily of the high-grade serous ovarian carcinoma histologic subtype, had significantly distinct differential abundances of the genera Brevibacterium (p < 0.001), Chloronema (p < 0.001), Facklamia (p < 0.001), Sutterella (p < 0.001), and Zymomonas (p < 0.001) when compared to the other study groups. These results suggest that plasma EOC-associated bacteria could be further exploited in follow-up studies to validate clinical applicability in disease screening, diagnostics, and risk stratification.
Additional Links: PMID-41726575
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@article {pmid41726575,
year = {2026},
author = {Mahoney, DE and Chalise, P and Pei, D and Griffard-Smith, R and Home, T and Pathak, HB and Umar, S and Godwin, AK},
title = {Distinguishing the significance of blood microbes in epithelial ovarian cancer.},
journal = {Gut microbes reports},
volume = {3},
number = {1},
pages = {},
pmid = {41726575},
issn = {2993-3935},
support = {P20 GM130423/GM/NIGMS NIH HHS/United States ; R01 CA260132/CA/NCI NIH HHS/United States ; },
abstract = {The human microbiome has generated growing interest in epithelial ovarian cancer (EOC) research, yet investigations of the blood microbiome remain sparse. This study explored plasma microbial signatures unique to EOC. We accessed 180 age/race/ethnicity-matched archival plasma samples from women with (1) EOC; (2) commonly diagnosed non-EOC solid tumors in women; (3) benign gynecologic conditions; and (4) age/race/ethnicity-matched controls. The microbial profiles of the plasma specimens were assessed using an amplicon-based sequencing method that targets the 16S rRNA gene in the bacterial genome. A stringent bioinformatic pipeline was applied to filter out suspicious bacterial contaminants at the genus level. Bioinformatic decontamination analysis removed 225 high-risk bacterial contaminants. The remaining 339 high-confidence bacteria were included in the final analysis for differential abundances in the plasma between the study groups. Women with EOC, which were primarily of the high-grade serous ovarian carcinoma histologic subtype, had significantly distinct differential abundances of the genera Brevibacterium (p < 0.001), Chloronema (p < 0.001), Facklamia (p < 0.001), Sutterella (p < 0.001), and Zymomonas (p < 0.001) when compared to the other study groups. These results suggest that plasma EOC-associated bacteria could be further exploited in follow-up studies to validate clinical applicability in disease screening, diagnostics, and risk stratification.},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
Pre-treatment endocrine-nutritional signatures predict clinical benefit from PD-1/PD-L1 blockade in hematologic malignancies.
Frontiers in nutrition, 12:1753660.
Hematologic malignancies pose significant global health burdens, with programmed cell death protein-1 (PD-1)/programmed cell death ligand 1 (PD-L1) inhibitors revolutionizing treatment in subtypes like classical Hodgkin lymphoma (cHL) and primary mediastinal large B-cell lymphoma (PMBCL), achieving high objective response rates (ORR). However, efficacy varies widely, with limited success in multiple myeloma (< 10% ORR) and leukemias, underscoring the need for better predictors beyond tumor-intrinsic biomarkers. This review highlights pre-treatment endocrine-nutritional signatures as key host factors influencing immunotherapy outcomes. Dysregulated hormones (cortisol, thyroid, sex steroids, insulin/insulin-like growth factor-1, adipokines) and nutritional status (vitamin D, zinc, protein-energy malnutrition, iron metabolism) modulate T-cell exhaustion, myeloid suppression, and tumor microenvironment dynamics, often leading to resistance. Evidence from cohorts shows hypercortisolism, hypothyroidism, insulin resistance, vitamin D deficiency, and hypoalbuminemia correlate with inferior ORR, progression-free survival, and overall survival, while thyroid immune-related adverse events and moderate obesity predict benefit. In hematologic contexts, marrow infiltration exacerbates these imbalances, explaining heterogeneous responses. Integrated signatures (e.g., Glasgow Prognostic Score, Prognostic Nutritional Index) offer superior prognostic value, enabling targeted interventions like vitamin D supplementation, metformin, or nutritional support to enhance immune checkpoint inhibitor efficacy. Mechanistic insights reveal convergence on mTOR/IFN-γ pathways and microbiome modulation. Translating these to clinical panels could personalize immunotherapy, addressing gaps in hematologic malignancies literature and improving outcomes in relapsed/refractory settings.
Additional Links: PMID-41726000
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@article {pmid41726000,
year = {2025},
author = {Huang, N and Guan, Y},
title = {Pre-treatment endocrine-nutritional signatures predict clinical benefit from PD-1/PD-L1 blockade in hematologic malignancies.},
journal = {Frontiers in nutrition},
volume = {12},
number = {},
pages = {1753660},
pmid = {41726000},
issn = {2296-861X},
abstract = {Hematologic malignancies pose significant global health burdens, with programmed cell death protein-1 (PD-1)/programmed cell death ligand 1 (PD-L1) inhibitors revolutionizing treatment in subtypes like classical Hodgkin lymphoma (cHL) and primary mediastinal large B-cell lymphoma (PMBCL), achieving high objective response rates (ORR). However, efficacy varies widely, with limited success in multiple myeloma (< 10% ORR) and leukemias, underscoring the need for better predictors beyond tumor-intrinsic biomarkers. This review highlights pre-treatment endocrine-nutritional signatures as key host factors influencing immunotherapy outcomes. Dysregulated hormones (cortisol, thyroid, sex steroids, insulin/insulin-like growth factor-1, adipokines) and nutritional status (vitamin D, zinc, protein-energy malnutrition, iron metabolism) modulate T-cell exhaustion, myeloid suppression, and tumor microenvironment dynamics, often leading to resistance. Evidence from cohorts shows hypercortisolism, hypothyroidism, insulin resistance, vitamin D deficiency, and hypoalbuminemia correlate with inferior ORR, progression-free survival, and overall survival, while thyroid immune-related adverse events and moderate obesity predict benefit. In hematologic contexts, marrow infiltration exacerbates these imbalances, explaining heterogeneous responses. Integrated signatures (e.g., Glasgow Prognostic Score, Prognostic Nutritional Index) offer superior prognostic value, enabling targeted interventions like vitamin D supplementation, metformin, or nutritional support to enhance immune checkpoint inhibitor efficacy. Mechanistic insights reveal convergence on mTOR/IFN-γ pathways and microbiome modulation. Translating these to clinical panels could personalize immunotherapy, addressing gaps in hematologic malignancies literature and improving outcomes in relapsed/refractory settings.},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
Global trends and future perspectives in autism spectrum disorder and gut microbiota research: a comprehensive bibliometric analysis.
Frontiers in neuroscience, 20:1607951.
BACKGROUND: Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental condition. Increasing studies examine whether gut microbiota alterations and the gut-brain axis are linked to ASD-relevant phenotypes. As the literature expands rapidly, a quantitative mapping is needed to clarify influential work and evolving themes.
OBJECTIVE: To map global research on ASD and the gut microbiota, identify major contributors and knowledge bases, and characterize thematic evolution and emerging fronts.
METHODS: We analyzed 1,391 English-language articles and reviews indexed in the Web of Science Core Collection (1999-2024). CiteSpace, VOSviewer, and R were used to evaluate publication trends, collaboration networks, co-citation structure, keyword clustering, and burst detection.
RESULTS: Publication output increased slowly before 2010 and accelerated after 2018. The United States and China were leading contributors and key collaboration hubs. The co-citation core was anchored by landmark experimental and translational studies, including work on microbiome-to-behavior links and microbiome-targeted interventions. Keyword clustering and timeline views highlighted three prominent thematic directions: fecal microbiota transplantation, Rett syndrome, and maternal immune activation. Recurrent and burst keywords emphasized the gut-brain axis, short-chain fatty acids, gastrointestinal symptoms, and oxidative stress. Recent burst terms, including obesity, major depressive disorder, and glutamate, suggest increasing connections to metabolic and broader psychiatric dimensions.
CONCLUSION: ASD-microbiome research has shifted from descriptive comparisons toward mechanism-oriented and intervention-relevant questions. Future progress will benefit from standardized protocols, longitudinal designs, and multi-omics integration, together with rigorously designed trials to evaluate microbiome-targeted strategies.
Additional Links: PMID-41725847
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Citation:
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@article {pmid41725847,
year = {2026},
author = {Liu, G and Chen, L and Guan, M and Xiao, N},
title = {Global trends and future perspectives in autism spectrum disorder and gut microbiota research: a comprehensive bibliometric analysis.},
journal = {Frontiers in neuroscience},
volume = {20},
number = {},
pages = {1607951},
pmid = {41725847},
issn = {1662-4548},
abstract = {BACKGROUND: Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental condition. Increasing studies examine whether gut microbiota alterations and the gut-brain axis are linked to ASD-relevant phenotypes. As the literature expands rapidly, a quantitative mapping is needed to clarify influential work and evolving themes.
OBJECTIVE: To map global research on ASD and the gut microbiota, identify major contributors and knowledge bases, and characterize thematic evolution and emerging fronts.
METHODS: We analyzed 1,391 English-language articles and reviews indexed in the Web of Science Core Collection (1999-2024). CiteSpace, VOSviewer, and R were used to evaluate publication trends, collaboration networks, co-citation structure, keyword clustering, and burst detection.
RESULTS: Publication output increased slowly before 2010 and accelerated after 2018. The United States and China were leading contributors and key collaboration hubs. The co-citation core was anchored by landmark experimental and translational studies, including work on microbiome-to-behavior links and microbiome-targeted interventions. Keyword clustering and timeline views highlighted three prominent thematic directions: fecal microbiota transplantation, Rett syndrome, and maternal immune activation. Recurrent and burst keywords emphasized the gut-brain axis, short-chain fatty acids, gastrointestinal symptoms, and oxidative stress. Recent burst terms, including obesity, major depressive disorder, and glutamate, suggest increasing connections to metabolic and broader psychiatric dimensions.
CONCLUSION: ASD-microbiome research has shifted from descriptive comparisons toward mechanism-oriented and intervention-relevant questions. Future progress will benefit from standardized protocols, longitudinal designs, and multi-omics integration, together with rigorously designed trials to evaluate microbiome-targeted strategies.},
}
RevDate: 2026-02-23
CmpDate: 2026-02-23
Synergistic remediation of Pb contamination in rice field soil with FeMg-LDH@Bentonite and compost: impacts on Pb bioavailability and soil environment.
Frontiers in microbiology, 17:1756444.
INTRODUCTION: Lead (Pb) contamination in paddy soils can degrade soil quality, increase plant Pb uptake, and disrupt soil microbial communities. This study evaluated integrated remediation using FeMg-LDH@Bentonite (FMLB) and compost, focusing on Pb bioavailability, plant uptake, and microbial community structure.
METHODS: A pot-based remediation experiment was conducted using Pb-contaminated paddy soil. FMLB and compost were applied at different mixing ratios. Pb bioavailability and soil Pb levels were assessed alongside plant uptake indicators. Soil microbial community structure and alpha-diversity were characterized (e.g., by 16S rRNA gene amplicon sequencing), and soil enzyme activities were measured to reflect soil biological functioning.
RESULTS: Pb contamination significantly altered soil properties, reduced soil quality, and impacted microbial diversity. Amendment application reduced Pb bioavailability across treatments, with the greatest reduction observed for the combined treatment of FMLB:compost = 3:7. This optimal combination not only decreased Pb concentrations and plant uptake potential, but also improved microbial indicators: bacterial community composition and α-diversity metrics shifted toward the original soil (OS) reference under identical pot conditions, and enzyme activities were enhanced.
DISCUSSION: Overall, combined application of FMLB and compost represents an environmentally sound and potentially cost-effective strategy for remediating Pb-contaminated paddy soils while improving soil fertility and microbial function. Importantly, microbiome responses and selected enzyme endpoints are interpreted as indicators associated with Pb stabilization and improved soil condition, rather than direct evidence of microbially mediated Pb transformation.
Additional Links: PMID-41725807
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Citation:
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@article {pmid41725807,
year = {2026},
author = {Guan, X and Bai, J and Yuan, XZ and Guo, JW and Liu, X},
title = {Synergistic remediation of Pb contamination in rice field soil with FeMg-LDH@Bentonite and compost: impacts on Pb bioavailability and soil environment.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1756444},
pmid = {41725807},
issn = {1664-302X},
abstract = {INTRODUCTION: Lead (Pb) contamination in paddy soils can degrade soil quality, increase plant Pb uptake, and disrupt soil microbial communities. This study evaluated integrated remediation using FeMg-LDH@Bentonite (FMLB) and compost, focusing on Pb bioavailability, plant uptake, and microbial community structure.
METHODS: A pot-based remediation experiment was conducted using Pb-contaminated paddy soil. FMLB and compost were applied at different mixing ratios. Pb bioavailability and soil Pb levels were assessed alongside plant uptake indicators. Soil microbial community structure and alpha-diversity were characterized (e.g., by 16S rRNA gene amplicon sequencing), and soil enzyme activities were measured to reflect soil biological functioning.
RESULTS: Pb contamination significantly altered soil properties, reduced soil quality, and impacted microbial diversity. Amendment application reduced Pb bioavailability across treatments, with the greatest reduction observed for the combined treatment of FMLB:compost = 3:7. This optimal combination not only decreased Pb concentrations and plant uptake potential, but also improved microbial indicators: bacterial community composition and α-diversity metrics shifted toward the original soil (OS) reference under identical pot conditions, and enzyme activities were enhanced.
DISCUSSION: Overall, combined application of FMLB and compost represents an environmentally sound and potentially cost-effective strategy for remediating Pb-contaminated paddy soils while improving soil fertility and microbial function. Importantly, microbiome responses and selected enzyme endpoints are interpreted as indicators associated with Pb stabilization and improved soil condition, rather than direct evidence of microbially mediated Pb transformation.},
}
RevDate: 2026-02-23
Glucuronolactone Promotes Mucin Sulfation to Alleviate Deoxynivalenol-Induced Intestinal Injury via Microbiota-Dependent and -Independent AHR Activation.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
Deoxynivalenol (DON), a prevalent trichothecene mycotoxin, poses a global threat to the gut health of both humans and livestock. This study investigates the protective effects and underlying mechanisms of glucuronolactone (GLU) against DON-induced intestinal injury. In a piglet model, GLU effectively alleviated DON-induced intestinal injury and inflammation. Transcriptomic analysis revealed that GLU promotes mucin sulfation, a critical process for fortifying the intestinal mucus barrier. On the one hand, integrated microbiome and metabolomics analyses uncovered that GLU increased probiotic Lactobacillus amylovorus abundance and luminal indole-3-acetic acid level, thereby facilitating mucin sulfation. On the other hand, GLU itself directly boosted mucin sulfation in a microbiota-independent manner. Mechanistically, both the microbiota-dependent and -independent pathways through which GLU promoted mucin sulfation converged on the activation of aryl hydrocarbon receptor (AHR). Activated AHR transcriptionally up-regulated the expression of the sulfotransferase GAL3ST3, which drove mucin sulfation. This study identifies GLU as a promising nutritional intervention against DON-induced intestinal injury and reveals AHR-mediated mucin sulfation as a vital mechanism for maintaining intestinal barrier homeostasis.
Additional Links: PMID-41725587
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@article {pmid41725587,
year = {2026},
author = {Cui, C and Zhang, B and Tang, J and Hou, J and Qiu, Y and Gao, K and Wang, L and Jiang, Z and Yang, X},
title = {Glucuronolactone Promotes Mucin Sulfation to Alleviate Deoxynivalenol-Induced Intestinal Injury via Microbiota-Dependent and -Independent AHR Activation.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e22912},
doi = {10.1002/advs.202522912},
pmid = {41725587},
issn = {2198-3844},
support = {2021YFD1300402//National Key R&D Program of China/ ; 2025A1515012362//Guangdong Basic and Applied Basic Research Foundation/ ; 2024CXTD14 2024CXTD22//Modern Agricultural Industrial Technology System Innovation Team of Guangdong Province/ ; R2023PY-JG013 R2020PY-JX007//Special Fund for Scientific Innovation Strategy-construction of High-Level Academy of Agriculture Science/ ; CARS-35//Earmarked Fund for China Agriculture Research System/ ; },
abstract = {Deoxynivalenol (DON), a prevalent trichothecene mycotoxin, poses a global threat to the gut health of both humans and livestock. This study investigates the protective effects and underlying mechanisms of glucuronolactone (GLU) against DON-induced intestinal injury. In a piglet model, GLU effectively alleviated DON-induced intestinal injury and inflammation. Transcriptomic analysis revealed that GLU promotes mucin sulfation, a critical process for fortifying the intestinal mucus barrier. On the one hand, integrated microbiome and metabolomics analyses uncovered that GLU increased probiotic Lactobacillus amylovorus abundance and luminal indole-3-acetic acid level, thereby facilitating mucin sulfation. On the other hand, GLU itself directly boosted mucin sulfation in a microbiota-independent manner. Mechanistically, both the microbiota-dependent and -independent pathways through which GLU promoted mucin sulfation converged on the activation of aryl hydrocarbon receptor (AHR). Activated AHR transcriptionally up-regulated the expression of the sulfotransferase GAL3ST3, which drove mucin sulfation. This study identifies GLU as a promising nutritional intervention against DON-induced intestinal injury and reveals AHR-mediated mucin sulfation as a vital mechanism for maintaining intestinal barrier homeostasis.},
}
RevDate: 2026-02-23
Commentary on Gut Microbiome-Metabolome Alterations in Advanced Parkinson's Disease With Motor Complications.
CNS neuroscience & therapeutics, 32(2):e70789.
Additional Links: PMID-41725434
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@article {pmid41725434,
year = {2026},
author = {Rashid, H},
title = {Commentary on Gut Microbiome-Metabolome Alterations in Advanced Parkinson's Disease With Motor Complications.},
journal = {CNS neuroscience & therapeutics},
volume = {32},
number = {2},
pages = {e70789},
doi = {10.1002/cns.70789},
pmid = {41725434},
issn = {1755-5949},
}
RevDate: 2026-02-23
Pharmacokinetics of Long-Acting Ampicillin and Its Impact on the Gut Microbiome and Resistome in Rhesus Macaques (Macaca mulatta).
Journal of veterinary pharmacology and therapeutics [Epub ahead of print].
Injectable antimicrobials with documented prolonged dosing intervals (> 48 h) for use in rhesus macaques are sparse. The objective of our study was to assess the pharmacokinetics, urine excretion, and effects on gut microbiome and resistome of intramuscular administered long-acting formulation of ampicillin (Albipen LA) in macaques. Four female rhesus macaques (Macaca mulatta) were administered intramuscularly 25 mg/kg anhydrous ampicillin (AMP-LA). Serial plasma samples were collected over a 72 h period and urine samples were collected over a 150 h period. Rectal swabs were collected over a 180-day period for microbiome and resistome analysis. Both plasma and urine samples were analyzed with ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). The pharmacokinetic parameters for AMP-LA ranged as follows: Cmax 1.3-10.3 μg/mL, T1/2 5.5-10.6 h, AUC0-∞ 52.5-135.4 μg h/mL. Post-administration, alpha diversity significantly decreased on Day 2 and maintained reduced up till Day 14. Sequence depth of beta-lactam resistance genes significantly increased on Day 2 after administration and then declined until Day 90. A dose of 25 mg/kg AMP-LA administered intramuscularly maintains a plasma concentration ≥ 0.25 μg/mL for up to 48 h. Therefore, administration of AMP-LA could be an effective treatment with a prolonged treatment interval for relevant organisms with short lasting effects on the intestinal microbiome and resistome.
Additional Links: PMID-41725112
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@article {pmid41725112,
year = {2026},
author = {Maaskant, A and van Geijlswijk, IM and Devreese, M and Cherlet, M and van Geest, LF and Wagenaar, JA and Langermans, JAM and Zomer, AL and Bakker, J and Gehring, R},
title = {Pharmacokinetics of Long-Acting Ampicillin and Its Impact on the Gut Microbiome and Resistome in Rhesus Macaques (Macaca mulatta).},
journal = {Journal of veterinary pharmacology and therapeutics},
volume = {},
number = {},
pages = {},
doi = {10.1111/jvp.70055},
pmid = {41725112},
issn = {1365-2885},
abstract = {Injectable antimicrobials with documented prolonged dosing intervals (> 48 h) for use in rhesus macaques are sparse. The objective of our study was to assess the pharmacokinetics, urine excretion, and effects on gut microbiome and resistome of intramuscular administered long-acting formulation of ampicillin (Albipen LA) in macaques. Four female rhesus macaques (Macaca mulatta) were administered intramuscularly 25 mg/kg anhydrous ampicillin (AMP-LA). Serial plasma samples were collected over a 72 h period and urine samples were collected over a 150 h period. Rectal swabs were collected over a 180-day period for microbiome and resistome analysis. Both plasma and urine samples were analyzed with ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). The pharmacokinetic parameters for AMP-LA ranged as follows: Cmax 1.3-10.3 μg/mL, T1/2 5.5-10.6 h, AUC0-∞ 52.5-135.4 μg h/mL. Post-administration, alpha diversity significantly decreased on Day 2 and maintained reduced up till Day 14. Sequence depth of beta-lactam resistance genes significantly increased on Day 2 after administration and then declined until Day 90. A dose of 25 mg/kg AMP-LA administered intramuscularly maintains a plasma concentration ≥ 0.25 μg/mL for up to 48 h. Therefore, administration of AMP-LA could be an effective treatment with a prolonged treatment interval for relevant organisms with short lasting effects on the intestinal microbiome and resistome.},
}
RevDate: 2026-02-22
CmpDate: 2026-02-22
Prostaglandin E2-EP4 Signaling at the Gut-Immune-Metabolic Interface: A Lipid Mediator Perspective on Obesity and Insulin Resistance.
Comprehensive Physiology, 16(1):e70099.
Despite advances in dietary and pharmacologic therapies, obesity rates continue to escalate globally. Emerging evidence implicates the gut-immune interface as a key determinant of metabolic dysfunction. This review highlights the prostaglandin E2 (PGE2) EP4 signaling axis as a pivotal mediator linking gut dysbiosis to systemic insulin resistance. In obesity, elevated COX-2-derived PGE2 reprograms the gut microbiota, depleting short-chain fatty acid (SCFA)-producing taxa and reducing regulatory T cell (Treg) homeostasis. The ensuing loss of intestinal integrity promotes metabolic endotoxemia and chronic low-grade inflammation, culminating in insulin resistance. Targeting the PGE2-EP4 microbiota Treg network through EP4 antagonists or microbiome restoration offers a promising therapeutic strategy to restore metabolic balance and prevent obesity associated complications.
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@article {pmid41725055,
year = {2026},
author = {Ganamurali, N and Sabarathinam, S},
title = {Prostaglandin E2-EP4 Signaling at the Gut-Immune-Metabolic Interface: A Lipid Mediator Perspective on Obesity and Insulin Resistance.},
journal = {Comprehensive Physiology},
volume = {16},
number = {1},
pages = {e70099},
doi = {10.1002/cph4.70099},
pmid = {41725055},
issn = {2040-4603},
mesh = {Humans ; *Obesity/metabolism/immunology ; *Insulin Resistance/physiology ; Animals ; *Receptors, Prostaglandin E, EP4 Subtype/metabolism ; Signal Transduction/physiology ; Gastrointestinal Microbiome/physiology ; *Dinoprostone/metabolism ; },
abstract = {Despite advances in dietary and pharmacologic therapies, obesity rates continue to escalate globally. Emerging evidence implicates the gut-immune interface as a key determinant of metabolic dysfunction. This review highlights the prostaglandin E2 (PGE2) EP4 signaling axis as a pivotal mediator linking gut dysbiosis to systemic insulin resistance. In obesity, elevated COX-2-derived PGE2 reprograms the gut microbiota, depleting short-chain fatty acid (SCFA)-producing taxa and reducing regulatory T cell (Treg) homeostasis. The ensuing loss of intestinal integrity promotes metabolic endotoxemia and chronic low-grade inflammation, culminating in insulin resistance. Targeting the PGE2-EP4 microbiota Treg network through EP4 antagonists or microbiome restoration offers a promising therapeutic strategy to restore metabolic balance and prevent obesity associated complications.},
}
MeSH Terms:
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Humans
*Obesity/metabolism/immunology
*Insulin Resistance/physiology
Animals
*Receptors, Prostaglandin E, EP4 Subtype/metabolism
Signal Transduction/physiology
Gastrointestinal Microbiome/physiology
*Dinoprostone/metabolism
RevDate: 2026-02-22
Mikania micrantha invasion restructures rhizosphere nitrogen cycling through enzyme activation, microbial recruitment, and allelopathic regulation.
Microbiome pii:10.1186/s40168-026-02334-8 [Epub ahead of print].
BACKGROUND: Plant invasions profoundly influence terrestrial ecosystems by reshaping nutrient cycling processes. However, the mechanisms through which invasive plants such as Mikania micrantha modulate soil nitrogen (N) cycling and microbial communities remain insufficiently explored. Moreover, comparative studies with indigenous congener are scarce, limiting insights into whether such effects reflect species-specific strategies or genus-wide traits. This study investigates how M. micrantha modulates nitrogen metabolic pathways and rhizosphere microecology using combined metagenomic and metabolomic analyses.
RESULTS: Integrated analyses revealed that M. micrantha established a distinctive "high total nitrogen-low mineral nitrogen" profile in the rhizosphere soil. Metagenomic profiling showed consistent enrichment of key ammonium assimilation enzymes, including glutamine synthetase and glutamate dehydrogenase, promoting enhanced incorporation of NH₄⁺ into organic nitrogen pools. In contrast, genes encoding nitrate reductase and nitrate transporters were significantly lower in relative abundance, limiting nitrate assimilation. Mikania micrantha also selectively enriched nitrogen-fixing microbes (notably rhizobia genera) and plant growth-promoting rhizobacteria (PGPR), thereby enhancing biological nitrogen fixation capacity. Metabolomic analysis further identified several allelopathic compounds in invaded soils at higher relative abundance, particularly epicatechin, which exhibited inhibitory effects on nitrifying bacteria. Compared with the congener Mikania cordata, which exerted weaker impacts on soil nitrogen cycling and microbial assembly, M. micrantha deployed a more comprehensive strategy integrating biochemical, microbial, and metabolic regulation.
CONCLUSIONS: These findings demonstrate that under greenhouse-controlled conditions, M. micrantha reconfigures rhizosphere nitrogen cycling through a multi-dimensional strategy that couples biochemical regulation, microbial recruitment, and metabolite-mediated interference, thereby suggesting a potential mechanism that may contribute to its ecological advantage in natural settings. Video Abstract.
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@article {pmid41725015,
year = {2026},
author = {Wang, R and Wang, Z and Liao, W and Wang, T and Su, Y},
title = {Mikania micrantha invasion restructures rhizosphere nitrogen cycling through enzyme activation, microbial recruitment, and allelopathic regulation.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02334-8},
pmid = {41725015},
issn = {2049-2618},
support = {31872670//National Natural Science Foundation of China/ ; 2021A1515010911//Guangdong Basic and Applied Basic Research Foundation/ ; 202206010107//Science and Technology Projects in Guangzhou/ ; JCYJ20210324141000001//Project of Department of Science and Technology of Shenzhen City, Guangdong, China/ ; },
abstract = {BACKGROUND: Plant invasions profoundly influence terrestrial ecosystems by reshaping nutrient cycling processes. However, the mechanisms through which invasive plants such as Mikania micrantha modulate soil nitrogen (N) cycling and microbial communities remain insufficiently explored. Moreover, comparative studies with indigenous congener are scarce, limiting insights into whether such effects reflect species-specific strategies or genus-wide traits. This study investigates how M. micrantha modulates nitrogen metabolic pathways and rhizosphere microecology using combined metagenomic and metabolomic analyses.
RESULTS: Integrated analyses revealed that M. micrantha established a distinctive "high total nitrogen-low mineral nitrogen" profile in the rhizosphere soil. Metagenomic profiling showed consistent enrichment of key ammonium assimilation enzymes, including glutamine synthetase and glutamate dehydrogenase, promoting enhanced incorporation of NH₄⁺ into organic nitrogen pools. In contrast, genes encoding nitrate reductase and nitrate transporters were significantly lower in relative abundance, limiting nitrate assimilation. Mikania micrantha also selectively enriched nitrogen-fixing microbes (notably rhizobia genera) and plant growth-promoting rhizobacteria (PGPR), thereby enhancing biological nitrogen fixation capacity. Metabolomic analysis further identified several allelopathic compounds in invaded soils at higher relative abundance, particularly epicatechin, which exhibited inhibitory effects on nitrifying bacteria. Compared with the congener Mikania cordata, which exerted weaker impacts on soil nitrogen cycling and microbial assembly, M. micrantha deployed a more comprehensive strategy integrating biochemical, microbial, and metabolic regulation.
CONCLUSIONS: These findings demonstrate that under greenhouse-controlled conditions, M. micrantha reconfigures rhizosphere nitrogen cycling through a multi-dimensional strategy that couples biochemical regulation, microbial recruitment, and metabolite-mediated interference, thereby suggesting a potential mechanism that may contribute to its ecological advantage in natural settings. Video Abstract.},
}
RevDate: 2026-02-24
CmpDate: 2026-02-24
Metagenomic analysis of the human gut virome reveals functional signatures and viral stability across hospitalized and non-hospitalized diarrheal and non-diarrheal individuals.
Gut pathogens, 18(1):.
BACKGROUND: The human gut virome is a fundamental yet understudied component of the intestinal microbiome. However, its taxonomic composition and functional potential in Latin American populations remain poorly understood, particularly under clinical stressors such as hospitalization and diarrhea conditions often linked to microbial dysbiosis.
METHODS: We conducted a hybrid metagenomic analysis of the human gut virome from 37 fecal samples: 10 from patients admitted to intensive care units (ICU), 13 from hospitalized patients outside the ICU (Non-ICU), and 14 from non-diarrheic individuals, including taxonomic and functional profiling of viruses and detection of viral auxiliary metabolic genes (vAMGs).
RESULTS: We identified 494 high-quality viral vOTUs, from which 37,619 ORFs were predicted. Taxonomically, Caudoviricetes and Intestiviridae were consistently present across all groups, supporting their role as part of a conserved core virome. Functionally, we identified 309 putative vAMGs spanning 90 functional categories, primarily related to metabolism and environmental information processing. Non-diarrheic individuals harbored a higher number and diversity of vAMGs compared to hospitalized groups (Kruskal-Wallis, p < 0.01), whereas ICU and Non-ICU patients showed reduced and more variable functional profiles. Beta diversity analysis revealed that diarrhea status, rather than hospitalization per se, was associated with modest but significant shifts in functional composition (PERMANOVA, R² = 0.047, p = 0.025), driven by quantitative changes in shared AMGs rather than the presence of unique functions. Notably, resistance-related vAMGs, including bacitracin transporters and Zinc D-Ala-D-Ala carboxypeptidase, were detected across samples, highlighting the potential of phages as mobile reservoirs of antibiotic resistance.
CONCLUSION: Together, our findings indicate that hospitalization and diarrhea do not markedly alter the taxonomic structure of the gut virome but are associated with modest shifts in viral functional potential. The maintenance of a stable viral community alongside variable AMG repertoires suggests that phages may modulate host-microbiome interactions primarily through functional fine-tuning rather than large-scale community restructuring. Our study provides evidence for the ecological resilience of the human gut virome and underscores the need to integrate viral communities into resistome research.
Additional Links: PMID-41725012
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Citation:
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@article {pmid41725012,
year = {2026},
author = {Ramírez, AL and Páez, L and Vega, L and Aya, V and Hernández, C and Luna, N and Muñoz, M and Patiño, LH and Ramírez, JD},
title = {Metagenomic analysis of the human gut virome reveals functional signatures and viral stability across hospitalized and non-hospitalized diarrheal and non-diarrheal individuals.},
journal = {Gut pathogens},
volume = {18},
number = {1},
pages = {},
pmid = {41725012},
issn = {1757-4749},
abstract = {BACKGROUND: The human gut virome is a fundamental yet understudied component of the intestinal microbiome. However, its taxonomic composition and functional potential in Latin American populations remain poorly understood, particularly under clinical stressors such as hospitalization and diarrhea conditions often linked to microbial dysbiosis.
METHODS: We conducted a hybrid metagenomic analysis of the human gut virome from 37 fecal samples: 10 from patients admitted to intensive care units (ICU), 13 from hospitalized patients outside the ICU (Non-ICU), and 14 from non-diarrheic individuals, including taxonomic and functional profiling of viruses and detection of viral auxiliary metabolic genes (vAMGs).
RESULTS: We identified 494 high-quality viral vOTUs, from which 37,619 ORFs were predicted. Taxonomically, Caudoviricetes and Intestiviridae were consistently present across all groups, supporting their role as part of a conserved core virome. Functionally, we identified 309 putative vAMGs spanning 90 functional categories, primarily related to metabolism and environmental information processing. Non-diarrheic individuals harbored a higher number and diversity of vAMGs compared to hospitalized groups (Kruskal-Wallis, p < 0.01), whereas ICU and Non-ICU patients showed reduced and more variable functional profiles. Beta diversity analysis revealed that diarrhea status, rather than hospitalization per se, was associated with modest but significant shifts in functional composition (PERMANOVA, R² = 0.047, p = 0.025), driven by quantitative changes in shared AMGs rather than the presence of unique functions. Notably, resistance-related vAMGs, including bacitracin transporters and Zinc D-Ala-D-Ala carboxypeptidase, were detected across samples, highlighting the potential of phages as mobile reservoirs of antibiotic resistance.
CONCLUSION: Together, our findings indicate that hospitalization and diarrhea do not markedly alter the taxonomic structure of the gut virome but are associated with modest shifts in viral functional potential. The maintenance of a stable viral community alongside variable AMG repertoires suggests that phages may modulate host-microbiome interactions primarily through functional fine-tuning rather than large-scale community restructuring. Our study provides evidence for the ecological resilience of the human gut virome and underscores the need to integrate viral communities into resistome research.},
}
RevDate: 2026-02-22
Soil antibiotic resistome in farmland exhibits higher diversity and horizontal transfer potential than adjacent pastureland in agro-pastoral ecotone.
Environmental microbiome pii:10.1186/s40793-026-00871-1 [Epub ahead of print].
BACKGROUND: Soil antibiotic resistant genes (ARGs) and mobile genetic elements (MGEs) are associated with agricultural land-use differences. However, assessing the soil antibiotic resistome differences between farmland and pastureland is often limited due to geographically unbalanced sample collection. Leveraging a typical agro-pastoral ecotone in northern China as the study model, we compared the soil microbiome and resistome between 15 adjacent farmland and pastureland pairs using metagenomic sequencing.
RESULTS: Results showed that farmland soils harbored higher soil ARG diversity (+ 2.75%), MGE diversity (+ 1.62%) and multidrug resistance-related gene abundance (+ 19.5%) than pastureland. Among them, genes conferring multidrug resistances were dominant in farmland, mainly carried by Pseudomonadota. While, vancomycin-resistant ARGs were dominant in pastureland, mainly carried by Actinomycetota. Metagenome-assembled genomes revealed that sul2 conferring sulfonamide resistance was shared by both Pseudomonadota and Acidobacteriota in farmland together with insertion sequence ISVsa3. Structural equation model analysis integrating with soil geography, pedology and microbiome data showed microbial community and soil properties were identified as major driving factors shaping soil antibiotic resistome diversity in both land-use contexts. MGE diversity showed a clear positive effect on ARG diversity in farmland soils but a minor effect in pastureland.
CONCLUSIONS: Together, this study elucidates the shared and distinguished soil antibiotic resistome pattern between farmland and pastureland, extending our understanding of driving factors in agricultural soil ARG contamination.
Additional Links: PMID-41724983
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@article {pmid41724983,
year = {2026},
author = {Yang, K and Li, J and Li, L and Fu, L and Liu, W and Jia, Z and Wang, Z and Wei, Z and Zhang, F},
title = {Soil antibiotic resistome in farmland exhibits higher diversity and horizontal transfer potential than adjacent pastureland in agro-pastoral ecotone.},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-026-00871-1},
pmid = {41724983},
issn = {2524-6372},
support = {CCPTZX2024QN03//National Center of Pratacultural Technology Innovation Special fund for innovation platform construction/ ; 42407171//National Natural Science Foundation of China/ ; 2025T180072, GZB20240311//China Postdoctoral Science Foundation/ ; },
abstract = {BACKGROUND: Soil antibiotic resistant genes (ARGs) and mobile genetic elements (MGEs) are associated with agricultural land-use differences. However, assessing the soil antibiotic resistome differences between farmland and pastureland is often limited due to geographically unbalanced sample collection. Leveraging a typical agro-pastoral ecotone in northern China as the study model, we compared the soil microbiome and resistome between 15 adjacent farmland and pastureland pairs using metagenomic sequencing.
RESULTS: Results showed that farmland soils harbored higher soil ARG diversity (+ 2.75%), MGE diversity (+ 1.62%) and multidrug resistance-related gene abundance (+ 19.5%) than pastureland. Among them, genes conferring multidrug resistances were dominant in farmland, mainly carried by Pseudomonadota. While, vancomycin-resistant ARGs were dominant in pastureland, mainly carried by Actinomycetota. Metagenome-assembled genomes revealed that sul2 conferring sulfonamide resistance was shared by both Pseudomonadota and Acidobacteriota in farmland together with insertion sequence ISVsa3. Structural equation model analysis integrating with soil geography, pedology and microbiome data showed microbial community and soil properties were identified as major driving factors shaping soil antibiotic resistome diversity in both land-use contexts. MGE diversity showed a clear positive effect on ARG diversity in farmland soils but a minor effect in pastureland.
CONCLUSIONS: Together, this study elucidates the shared and distinguished soil antibiotic resistome pattern between farmland and pastureland, extending our understanding of driving factors in agricultural soil ARG contamination.},
}
RevDate: 2026-02-22
CmpDate: 2026-02-22
Immobilization of a biostimulator microbial consortium on bacterial cellulose and its effect on onion growth, soil nutrient status and the microbial community.
World journal of microbiology & biotechnology, 42(3):.
The immobilization of plant growth-promoting rhizobacteria (PGPR) in biodegradable polymeric networks is a promising strategy for protecting them from environmental stresses and optimizing their plant-beneficial functions. In this study, a microbial consortium of Pseudomonas stutzeri and Beijerinckia mobilis was immobilized in bacterial cellulose (BC) produced by Komagataeibacter xylinus. Its efficacy was evaluated in onion (Allium cepa) under three treatments: uninoculated control, free cells, and immobilized cells, during a field trial conducted in the 2025 winter cropping season at El-Kharga Oasis, New Valley Governorate, Egypt. Both inoculation forms significantly (P < 0.05) enhanced plant growth, nutrient uptake, and soil fertility, with immobilized cells increasing bulb yield by 44.9% over the control and outperforming free cells. Treatments elevated N, P, K levels in bulbs and soil, with immobilized cells showing superior nutrient mobilization. The microbial diversity in the onion rhizosphere was assessed at harvest. Ecological diversity indices revealed that bacterial treatments, especially in immobilized form, were associated with a short-term reduction in overall microbial diversity, reflecting selective enrichment of plant-beneficial taxa while suppressing non-beneficial competitors. This functional shift enhanced rhizosphere efficiency without long-term detriment to soil health, as confirmed by post-harvest observations. The novelty of this work lies in the field-scale validation of BC as a biodegradable, highly porous carrier that protects PGPR under arid conditions while simultaneously modulating rhizosphere communities. This study highlights microbial immobilization in BC as a robust, eco-friendly approach to enhance crop yield and soil nutrient dynamics, offering a scalable strategy for sustainable agriculture. Photo 1 Graphical illustration showing PGPR immobilization in biocellulose and its effect on onion growth and nutrient uptake through microbiome modulation.
Additional Links: PMID-41724893
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@article {pmid41724893,
year = {2026},
author = {Yaseen, R},
title = {Immobilization of a biostimulator microbial consortium on bacterial cellulose and its effect on onion growth, soil nutrient status and the microbial community.},
journal = {World journal of microbiology & biotechnology},
volume = {42},
number = {3},
pages = {},
pmid = {41724893},
issn = {1573-0972},
mesh = {*Onions/growth & development/microbiology ; *Cellulose/metabolism ; *Soil Microbiology ; *Soil/chemistry ; *Microbial Consortia/physiology ; Rhizosphere ; Bacteria/metabolism/classification ; Nutrients/analysis/metabolism ; Egypt ; Microbiota ; Cells, Immobilized ; Plant Roots/microbiology/growth & development ; },
abstract = {The immobilization of plant growth-promoting rhizobacteria (PGPR) in biodegradable polymeric networks is a promising strategy for protecting them from environmental stresses and optimizing their plant-beneficial functions. In this study, a microbial consortium of Pseudomonas stutzeri and Beijerinckia mobilis was immobilized in bacterial cellulose (BC) produced by Komagataeibacter xylinus. Its efficacy was evaluated in onion (Allium cepa) under three treatments: uninoculated control, free cells, and immobilized cells, during a field trial conducted in the 2025 winter cropping season at El-Kharga Oasis, New Valley Governorate, Egypt. Both inoculation forms significantly (P < 0.05) enhanced plant growth, nutrient uptake, and soil fertility, with immobilized cells increasing bulb yield by 44.9% over the control and outperforming free cells. Treatments elevated N, P, K levels in bulbs and soil, with immobilized cells showing superior nutrient mobilization. The microbial diversity in the onion rhizosphere was assessed at harvest. Ecological diversity indices revealed that bacterial treatments, especially in immobilized form, were associated with a short-term reduction in overall microbial diversity, reflecting selective enrichment of plant-beneficial taxa while suppressing non-beneficial competitors. This functional shift enhanced rhizosphere efficiency without long-term detriment to soil health, as confirmed by post-harvest observations. The novelty of this work lies in the field-scale validation of BC as a biodegradable, highly porous carrier that protects PGPR under arid conditions while simultaneously modulating rhizosphere communities. This study highlights microbial immobilization in BC as a robust, eco-friendly approach to enhance crop yield and soil nutrient dynamics, offering a scalable strategy for sustainable agriculture. Photo 1 Graphical illustration showing PGPR immobilization in biocellulose and its effect on onion growth and nutrient uptake through microbiome modulation.},
}
MeSH Terms:
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*Onions/growth & development/microbiology
*Cellulose/metabolism
*Soil Microbiology
*Soil/chemistry
*Microbial Consortia/physiology
Rhizosphere
Bacteria/metabolism/classification
Nutrients/analysis/metabolism
Egypt
Microbiota
Cells, Immobilized
Plant Roots/microbiology/growth & development
RevDate: 2026-02-22
Methamphetamine induces long-lasting dysbiosis of the gut microbiota.
Molecular psychiatry [Epub ahead of print].
As a highly addictive and neurotoxic stimulant, methamphetamine poses a severe threat to public psychological well-being and social security. Dysbiosis of gut flora is presumed to be a potential mechanism for methamphetamine habituation. To test this hypothesis, we conducted a cross-species study to analyze the enduring effects of methamphetamine administration on the gut microbiome. Either in an abstinent cohort or sensitized mice, the microbial community remained distinct from controls even after a long-term methamphetamine withdrawal, establishing an emerging homeostasis through extensive interactions of symbionts. The dysbiosis was correlated to the duration of MA abuse. Within the discriminant genera, those in the order Clostridiales exhibited coordinated changes across hosts and functionally reshaped the gut flora, potentially contributing to recurring relapse of drug usage. These findings help comprehend the long-term detriment caused by methamphetamine and underscore the translational implications of leveraging gut microbiome analysis to combat MA-related criminal activities.
Additional Links: PMID-41724803
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@article {pmid41724803,
year = {2026},
author = {Ding, N and Zhu, S and Yue, L and Zhang, L and Liu, L and Wang, Q and Wang, C and Gao, Y and Yan, J and Tong, S and Chen, F and Sun, J and Zhang, J},
title = {Methamphetamine induces long-lasting dysbiosis of the gut microbiota.},
journal = {Molecular psychiatry},
volume = {},
number = {},
pages = {},
pmid = {41724803},
issn = {1476-5578},
support = {31401172//National Natural Science Foundation of China (National Science Foundation of China)/ ; 82371780//National Natural Science Foundation of China (National Science Foundation of China)/ ; 81401867//National Natural Science Foundation of China (National Science Foundation of China)/ ; 82204645//National Natural Science Foundation of China (National Science Foundation of China)/ ; U2202211//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
abstract = {As a highly addictive and neurotoxic stimulant, methamphetamine poses a severe threat to public psychological well-being and social security. Dysbiosis of gut flora is presumed to be a potential mechanism for methamphetamine habituation. To test this hypothesis, we conducted a cross-species study to analyze the enduring effects of methamphetamine administration on the gut microbiome. Either in an abstinent cohort or sensitized mice, the microbial community remained distinct from controls even after a long-term methamphetamine withdrawal, establishing an emerging homeostasis through extensive interactions of symbionts. The dysbiosis was correlated to the duration of MA abuse. Within the discriminant genera, those in the order Clostridiales exhibited coordinated changes across hosts and functionally reshaped the gut flora, potentially contributing to recurring relapse of drug usage. These findings help comprehend the long-term detriment caused by methamphetamine and underscore the translational implications of leveraging gut microbiome analysis to combat MA-related criminal activities.},
}
RevDate: 2026-02-22
Pseudolysogeny-mediated evolutionary trade-offs favor phage therapy by limiting antibiotic resistance and virulence in Cutibacterium acnes.
Scientific reports pii:10.1038/s41598-026-40701-5 [Epub ahead of print].
Phage therapy has mostly focused on strictly lytic phages, yet the ecological and evolutionary implications of pseudolysogeny remain poorly understood. Pseudolysogeny-where a phage genome persists in a non-integrated, latent state within the host-has been largely overlooked due to concerns about therapeutic efficacy. Here, we demonstrate that pseudolysogeny in Cutibacterium acnes confers superinfection resistance but imposes substantial fitness costs, including reduced biofilm formation, impaired interspecies competitiveness, and reversal of antibiotic resistance. Pseudolysogenic phages were also capable of killing starved C. acnes cells through direct lytic replication. No evidence of transduction of clindamycin resistance by these phages was detected. In a 3-month proof-of-concept study, topical application of a pseudolysogenic phage significantly reduced C. acnes abundance, acne lesions, and inflammation, with no adverse effects and persistence of viable phages post-treatment. Importantly, no phage-resistant C. acnes clones were detected during the in vivo study, likely due to the evolutionary trade-offs associated with pseudolysogeny that diminish the bacterial ecological fitness. These findings highlight pseudolysogeny as a mechanism that can be leveraged to enhance phage therapy outcomes while maintaining microbiome stability and limiting antibiotic resistance evolution.
Additional Links: PMID-41724747
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@article {pmid41724747,
year = {2026},
author = {Trejo-Hernández, A and Checa, A and Quijada-Ibarra, R and Sepúlveda-Gutíerrez, P and Soto, S and Andrade-Domínguez, A},
title = {Pseudolysogeny-mediated evolutionary trade-offs favor phage therapy by limiting antibiotic resistance and virulence in Cutibacterium acnes.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-40701-5},
pmid = {41724747},
issn = {2045-2322},
abstract = {Phage therapy has mostly focused on strictly lytic phages, yet the ecological and evolutionary implications of pseudolysogeny remain poorly understood. Pseudolysogeny-where a phage genome persists in a non-integrated, latent state within the host-has been largely overlooked due to concerns about therapeutic efficacy. Here, we demonstrate that pseudolysogeny in Cutibacterium acnes confers superinfection resistance but imposes substantial fitness costs, including reduced biofilm formation, impaired interspecies competitiveness, and reversal of antibiotic resistance. Pseudolysogenic phages were also capable of killing starved C. acnes cells through direct lytic replication. No evidence of transduction of clindamycin resistance by these phages was detected. In a 3-month proof-of-concept study, topical application of a pseudolysogenic phage significantly reduced C. acnes abundance, acne lesions, and inflammation, with no adverse effects and persistence of viable phages post-treatment. Importantly, no phage-resistant C. acnes clones were detected during the in vivo study, likely due to the evolutionary trade-offs associated with pseudolysogeny that diminish the bacterial ecological fitness. These findings highlight pseudolysogeny as a mechanism that can be leveraged to enhance phage therapy outcomes while maintaining microbiome stability and limiting antibiotic resistance evolution.},
}
RevDate: 2026-02-22
Exploration of the Tumor Transcriptomic and Immune Landscape Following Repeated Transurethral Resection in Non-Muscle-Invasive Bladder Cancer.
Clinical genitourinary cancer pii:S1558-7673(26)00013-3 [Epub ahead of print].
OBJECTIVE: To investigate the associations of repeated transurethral resection of bladder tumor (TURBT) and BCG treatment with molecular, immunological, and microbial landscapes of nonmuscle-invasive bladder cancer (NMIBC).
METHODS: Tumor and matched normal tissues from 24 NMIBC patients (primary TURBT, n = 12; repeated TURBT, n = 12) underwent RNA sequencing for transcriptomic and immune repertoire analyses. Urine samples were analyzed by 16S rRNA sequencing to characterize the urinary microbiome. Patients in the repeated TURBT group were further stratified by BCG treatment status (BCG-treated, n = 5; non-BCG, n = 7).
RESULTS: Repeated TURBT was associated with differences in transcriptomic reprogramming, immune remodeling, and urinary microbiome profiles compared with primary TURBT. Compared with primary tumors, repeated tumors exhibited a transcriptional shift from hypoxia- and metabolism-related pathways toward proliferative cell cycle programs and partial restoration of T and B cell receptor diversity. Microsatellite instability scores did not differ significantly between groups. BCG treatment primarily enhanced dendritic cell activation, reflecting innate immune stimulation without affecting adaptive repertoires. Urinary microbiome analysis revealed increased heterogeneity, with cyanobacteriota and Corynebacterium detected exclusively in patients who underwent repeated TURBT without BCG treatment.
CONCLUSION: In this exploratory cohort, repeated TURBT was associated with coordinated transcriptomic, immunologic, and microbial features in NMIBC. These preliminary findings suggest that surgical history may influence tumor-associated molecular and immune characteristics and warrant further investigation in larger, longitudinal studies.
Additional Links: PMID-41724651
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@article {pmid41724651,
year = {2026},
author = {Seo, J and Park, JM and Park, DJ and Seo, I and Kwon, SY},
title = {Exploration of the Tumor Transcriptomic and Immune Landscape Following Repeated Transurethral Resection in Non-Muscle-Invasive Bladder Cancer.},
journal = {Clinical genitourinary cancer},
volume = {},
number = {},
pages = {102513},
doi = {10.1016/j.clgc.2026.102513},
pmid = {41724651},
issn = {1938-0682},
abstract = {OBJECTIVE: To investigate the associations of repeated transurethral resection of bladder tumor (TURBT) and BCG treatment with molecular, immunological, and microbial landscapes of nonmuscle-invasive bladder cancer (NMIBC).
METHODS: Tumor and matched normal tissues from 24 NMIBC patients (primary TURBT, n = 12; repeated TURBT, n = 12) underwent RNA sequencing for transcriptomic and immune repertoire analyses. Urine samples were analyzed by 16S rRNA sequencing to characterize the urinary microbiome. Patients in the repeated TURBT group were further stratified by BCG treatment status (BCG-treated, n = 5; non-BCG, n = 7).
RESULTS: Repeated TURBT was associated with differences in transcriptomic reprogramming, immune remodeling, and urinary microbiome profiles compared with primary TURBT. Compared with primary tumors, repeated tumors exhibited a transcriptional shift from hypoxia- and metabolism-related pathways toward proliferative cell cycle programs and partial restoration of T and B cell receptor diversity. Microsatellite instability scores did not differ significantly between groups. BCG treatment primarily enhanced dendritic cell activation, reflecting innate immune stimulation without affecting adaptive repertoires. Urinary microbiome analysis revealed increased heterogeneity, with cyanobacteriota and Corynebacterium detected exclusively in patients who underwent repeated TURBT without BCG treatment.
CONCLUSION: In this exploratory cohort, repeated TURBT was associated with coordinated transcriptomic, immunologic, and microbial features in NMIBC. These preliminary findings suggest that surgical history may influence tumor-associated molecular and immune characteristics and warrant further investigation in larger, longitudinal studies.},
}
RevDate: 2026-02-22
Mixed Evidence for Impact of Early Infant Gut Microbiome and Later Development of Autism Spectrum Disorder in the MARBLES Prospective Cohort Study.
Autism research : official journal of the International Society for Autism Research [Epub ahead of print].
This study investigated the relationship between early infant gut microbiome composition and subsequent neurodevelopmental outcomes. Fecal samples from children in the markers of autism risks in babies-learning early signs (MARBLES) study, a cohort with elevated likelihood of autism, were collected between 0 and 7 months of age and analyzed using 16S rRNA sequencing to evaluate whether the gut microbial composition during early infancy is associated with later neurodevelopmental diagnoses. Clinical classification as autism spectrum disorder (ASD), non-typically developing without ASD (non-TD), or typically developing (TD) was completed around 36 months of age using gold-standard assessment tools. Overall, no significant differences in alpha diversity or beta diversity, nor any differentially abundant bacterial taxa, were found between groups of infants who developed ASD or non-TD compared to those who went on to have TD. Nonetheless, our findings highlight some early differences in gut microbial composition during infancy that may relate to later neurodevelopmental outcomes. Before adjusting for multiple comparisons, infants who later developed ASD had slightly lower levels of Veillonella and Flavonifractor genera compared to children who were later found to be TD. These results suggest specific bacterial taxa may already differentiate in early infancy, but may be more subtle than other factors, such as mode of delivery and diet during early infancy. To understand longitudinal trajectories of the gut microbiome in association with later neurodevelopment, future studies should include a larger cohort to detect smaller effect sizes or investigate later time points in infancy.
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@article {pmid41724596,
year = {2026},
author = {Sotelo-Orozco, J and Taft, DH and Al-Oboudi, J and Baikie, BC and Lake, C and Miller, M and Mills, DA and Tancredi, DJ and Schmidt, RJ and Hertz-Picciotto, I and Bennett, DH},
title = {Mixed Evidence for Impact of Early Infant Gut Microbiome and Later Development of Autism Spectrum Disorder in the MARBLES Prospective Cohort Study.},
journal = {Autism research : official journal of the International Society for Autism Research},
volume = {},
number = {},
pages = {e70207},
doi = {10.1002/aur.70207},
pmid = {41724596},
issn = {1939-3806},
support = {P01ES11269/NH/NIH HHS/United States ; R01ES020392/NH/NIH HHS/United States ; R01ES028089/NH/NIH HHS/United States ; P30ES023513/NH/NIH HHS/United States ; R/U24ES028533/NH/NIH HHS/United States ; P50HD103526//Eunice Kennedy Shriver National Institute of Child Health and Human Development/ ; SFARI #863967, RJS//Simons Foundation Autism Research Initiative/ ; RD-829388//U.S. Environmental Protection Agency/ ; RD-833292//U.S. Environmental Protection Agency/ ; //Intellectual and Developmental Disabilities Research Center/ ; },
abstract = {This study investigated the relationship between early infant gut microbiome composition and subsequent neurodevelopmental outcomes. Fecal samples from children in the markers of autism risks in babies-learning early signs (MARBLES) study, a cohort with elevated likelihood of autism, were collected between 0 and 7 months of age and analyzed using 16S rRNA sequencing to evaluate whether the gut microbial composition during early infancy is associated with later neurodevelopmental diagnoses. Clinical classification as autism spectrum disorder (ASD), non-typically developing without ASD (non-TD), or typically developing (TD) was completed around 36 months of age using gold-standard assessment tools. Overall, no significant differences in alpha diversity or beta diversity, nor any differentially abundant bacterial taxa, were found between groups of infants who developed ASD or non-TD compared to those who went on to have TD. Nonetheless, our findings highlight some early differences in gut microbial composition during infancy that may relate to later neurodevelopmental outcomes. Before adjusting for multiple comparisons, infants who later developed ASD had slightly lower levels of Veillonella and Flavonifractor genera compared to children who were later found to be TD. These results suggest specific bacterial taxa may already differentiate in early infancy, but may be more subtle than other factors, such as mode of delivery and diet during early infancy. To understand longitudinal trajectories of the gut microbiome in association with later neurodevelopment, future studies should include a larger cohort to detect smaller effect sizes or investigate later time points in infancy.},
}
RevDate: 2026-02-24
Immunotherapy in triple-negative breast cancer: From molecular mechanisms to precision medicine-overcoming resistance and optimizing clinical outcomes.
Critical reviews in oncology/hematology, 221:105174 pii:S1040-8428(26)00061-2 [Epub ahead of print].
Triple-negative breast cancer (TNBC) is the most violent type of breast cancer, in which estrogen receptors (ER), progesterone receptors (PR), and human epidermal growth factor receptor 2 (HER2) are not expressed, and with which has a disproportionately high poor survival rate. Recent developments in immuno-oncology have radically changed the treatment of TNBC based on its characteristic immunogenic pathophysiology such as high genomic instability, high tumour mutational burden (TMB), homologous recombination deficiency (HRD), and high tumour-infiltrating lymphocytes (TILs). Chemo-immunotherapy with pembrolizumab has become the first to show the ultimate overall survival advantage in the early-stage TNBC (KEYNOTE-522) with 65 % pathologic complete response (pCR) and 86.6 % 5-year survival, establishing a novel standard-of-care. Nevertheless, intrinsic or acquired resistance to immune checkpoint blockade (ICB) by tumour-intrinsic signalling (Wnt/β-catenin, PI3K/AKT/mTOR activation, loss of antigen-presentation) and suppressive tumour microenvironmental interactions between myeloid-derived suppressor cells (MDSCs), regulatory T cells (Tregs), and desmoplastic cancer-associated fibroblasts (CAFs) occur in 40-50 % of patients. Mechanistically rational precision medicine strategies to these barriers are currently in rapid development, such as synergistic combinations of poly (ADP-ribose) polymerase (PARP) inhibitors and checkpoint blockades, dual-checkpoint therapy (PD-1/CTLA-4; PD-1/LAG-3), CD40-based myeloid reprogramming and metabolic checkpoint inhibitor targeting lactate transport and glycolysis. Immunomodulatory delivery systems based on nanotechnology, artificial-intelligence-directed biomarker stratification, have become the next-generation systems to optimize treatment personalization, allow real-time resistance prediction, and extend durable immune control. Also, the neoantigen-mRNA vaccines and gut microbiome modulation are broadening the clinical perspective to build enduring immunologic memory and negate metastatic relapse. Mechanistic insights alongside multi-omics, computational, and biologic innovation are making a paradigm shift in TNBC- once historically fatal, a disease that could be controlled and cured. Further development of the predictive biomarkers, equity of access plans and avoidance of immune toxicity will be central to universal implementation of these immunotherapy advances.
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@article {pmid41724338,
year = {2026},
author = {Chatterjee, A and Chakraborty, A and Chatterjee, S and Pal, S},
title = {Immunotherapy in triple-negative breast cancer: From molecular mechanisms to precision medicine-overcoming resistance and optimizing clinical outcomes.},
journal = {Critical reviews in oncology/hematology},
volume = {221},
number = {},
pages = {105174},
doi = {10.1016/j.critrevonc.2026.105174},
pmid = {41724338},
issn = {1879-0461},
abstract = {Triple-negative breast cancer (TNBC) is the most violent type of breast cancer, in which estrogen receptors (ER), progesterone receptors (PR), and human epidermal growth factor receptor 2 (HER2) are not expressed, and with which has a disproportionately high poor survival rate. Recent developments in immuno-oncology have radically changed the treatment of TNBC based on its characteristic immunogenic pathophysiology such as high genomic instability, high tumour mutational burden (TMB), homologous recombination deficiency (HRD), and high tumour-infiltrating lymphocytes (TILs). Chemo-immunotherapy with pembrolizumab has become the first to show the ultimate overall survival advantage in the early-stage TNBC (KEYNOTE-522) with 65 % pathologic complete response (pCR) and 86.6 % 5-year survival, establishing a novel standard-of-care. Nevertheless, intrinsic or acquired resistance to immune checkpoint blockade (ICB) by tumour-intrinsic signalling (Wnt/β-catenin, PI3K/AKT/mTOR activation, loss of antigen-presentation) and suppressive tumour microenvironmental interactions between myeloid-derived suppressor cells (MDSCs), regulatory T cells (Tregs), and desmoplastic cancer-associated fibroblasts (CAFs) occur in 40-50 % of patients. Mechanistically rational precision medicine strategies to these barriers are currently in rapid development, such as synergistic combinations of poly (ADP-ribose) polymerase (PARP) inhibitors and checkpoint blockades, dual-checkpoint therapy (PD-1/CTLA-4; PD-1/LAG-3), CD40-based myeloid reprogramming and metabolic checkpoint inhibitor targeting lactate transport and glycolysis. Immunomodulatory delivery systems based on nanotechnology, artificial-intelligence-directed biomarker stratification, have become the next-generation systems to optimize treatment personalization, allow real-time resistance prediction, and extend durable immune control. Also, the neoantigen-mRNA vaccines and gut microbiome modulation are broadening the clinical perspective to build enduring immunologic memory and negate metastatic relapse. Mechanistic insights alongside multi-omics, computational, and biologic innovation are making a paradigm shift in TNBC- once historically fatal, a disease that could be controlled and cured. Further development of the predictive biomarkers, equity of access plans and avoidance of immune toxicity will be central to universal implementation of these immunotherapy advances.},
}
RevDate: 2026-02-22
Microbiome- metabolome signatures and Behavioral alterations in a progressive MPTP-induced mouse model of Parkinson's disease.
Experimental neurology pii:S0014-4886(26)00064-6 [Epub ahead of print].
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuronal loss, motor deficits, and systemic metabolic dysfunction. Using a chronic MPTP-induced C57BL/6 mouse model, we integrated behavioral, transcriptional, metabolomic, and microbiome analyses to investigate gut-metabolite-brain interactions in PD. MPTP-treated mice exhibited significant motor and non-motor impairments alongside increased α-synuclein and inflammatory markers in the midbrain. Untargeted LC-MS metabolomics revealed differential enrichment of host- and microbiome-derived metabolites, including altered arginine/proline, sphingolipid, tryptophan, and riboflavin metabolism. 16S rRNA sequencing demonstrated decreased Firmicutes/Bacteroidetes ratio and enrichment of lipopolysaccharide-producing taxa, functionally linked to amino-acid metabolism via correlation network analysis. These data define a coordinated gut-metabolite-brain axis underpinning PD pathology, highlighting microbiome-derived circulating metabolites as potential early biomarkers and therapeutic targets. While these findings are derived from a toxin-based, male-only PD model, they delineate robust gut-metabolite-brain signatures that provide a strong framework for future validation in α-synucleinopathy models and mixed-sex cohorts.
Additional Links: PMID-41724229
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@article {pmid41724229,
year = {2026},
author = {Das, A and Das, R and Das, A and Aich, P},
title = {Microbiome- metabolome signatures and Behavioral alterations in a progressive MPTP-induced mouse model of Parkinson's disease.},
journal = {Experimental neurology},
volume = {},
number = {},
pages = {115701},
doi = {10.1016/j.expneurol.2026.115701},
pmid = {41724229},
issn = {1090-2430},
abstract = {Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuronal loss, motor deficits, and systemic metabolic dysfunction. Using a chronic MPTP-induced C57BL/6 mouse model, we integrated behavioral, transcriptional, metabolomic, and microbiome analyses to investigate gut-metabolite-brain interactions in PD. MPTP-treated mice exhibited significant motor and non-motor impairments alongside increased α-synuclein and inflammatory markers in the midbrain. Untargeted LC-MS metabolomics revealed differential enrichment of host- and microbiome-derived metabolites, including altered arginine/proline, sphingolipid, tryptophan, and riboflavin metabolism. 16S rRNA sequencing demonstrated decreased Firmicutes/Bacteroidetes ratio and enrichment of lipopolysaccharide-producing taxa, functionally linked to amino-acid metabolism via correlation network analysis. These data define a coordinated gut-metabolite-brain axis underpinning PD pathology, highlighting microbiome-derived circulating metabolites as potential early biomarkers and therapeutic targets. While these findings are derived from a toxin-based, male-only PD model, they delineate robust gut-metabolite-brain signatures that provide a strong framework for future validation in α-synucleinopathy models and mixed-sex cohorts.},
}
RevDate: 2026-02-22
What is the nature of sleep and circadian rhythm health on gastrointestinal microbiota? A systematic review of studies in humans.
Sleep medicine reviews, 86:102256 pii:S1087-0792(26)00028-6 [Epub ahead of print].
This systematic review synthesized findings from 41 human studies across the lifespan published between 2016 and 2025 examining associations of multidimensional sleep and circadian rhythm health with the gut microbiome (GM). The studies include experimental and observational designs of generally healthy participants, measuring sleep and circadian dimensions such as duration, quality, insomnia, and circadian disruptions (e.g., shift work). Results suggest sleep truncation, disturbances, and circadian misalignment may be linked to GM composition and function, though results were mixed on microbial diversity. The heterogeneous evidence suggests that the microbial family Oscillospiraceae/Ruminococcaceae is often associated with sleep and circadian metrics, warranting rigorous inquiry of taxa within this family. Functional outputs of the GM were infrequently assessed, but when measured, identified functions in amino acid and fatty acid metabolism, and vitamin, hormone/neurotransmitter, phosphate, short-chain fatty acid, and bile acid pathways. Inconsistencies in findings may reflect differing analytical methods, participants' age, health status, and lifestyle (e.g., diet, physical activity). Future investigations should prioritize longitudinal and experimental, multi-omics studies to clarify causal pathways and assess interventions, especially in populations with sleep disruption. Findings underscore the potential for sleep and circadian interventions to support GM balance and improve health outcomes.
Additional Links: PMID-41724023
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@article {pmid41724023,
year = {2026},
author = {Olson, M and Withrow, D and Koelbel, M and Southworth, G and Phan, A and Wright, KP and Whisner, CM and Petrov, ME},
title = {What is the nature of sleep and circadian rhythm health on gastrointestinal microbiota? A systematic review of studies in humans.},
journal = {Sleep medicine reviews},
volume = {86},
number = {},
pages = {102256},
doi = {10.1016/j.smrv.2026.102256},
pmid = {41724023},
issn = {1532-2955},
abstract = {This systematic review synthesized findings from 41 human studies across the lifespan published between 2016 and 2025 examining associations of multidimensional sleep and circadian rhythm health with the gut microbiome (GM). The studies include experimental and observational designs of generally healthy participants, measuring sleep and circadian dimensions such as duration, quality, insomnia, and circadian disruptions (e.g., shift work). Results suggest sleep truncation, disturbances, and circadian misalignment may be linked to GM composition and function, though results were mixed on microbial diversity. The heterogeneous evidence suggests that the microbial family Oscillospiraceae/Ruminococcaceae is often associated with sleep and circadian metrics, warranting rigorous inquiry of taxa within this family. Functional outputs of the GM were infrequently assessed, but when measured, identified functions in amino acid and fatty acid metabolism, and vitamin, hormone/neurotransmitter, phosphate, short-chain fatty acid, and bile acid pathways. Inconsistencies in findings may reflect differing analytical methods, participants' age, health status, and lifestyle (e.g., diet, physical activity). Future investigations should prioritize longitudinal and experimental, multi-omics studies to clarify causal pathways and assess interventions, especially in populations with sleep disruption. Findings underscore the potential for sleep and circadian interventions to support GM balance and improve health outcomes.},
}
RevDate: 2026-02-22
Honey microbiome as a source of bioactive metabolites: the role of the microorganisms and the influence of physicochemical parameters.
Journal of chromatography. A, 1772:466820 pii:S0021-9673(26)00150-0 [Epub ahead of print].
Beyond its nutritional and therapeutic properties, honey contains a unique microbiome that may also function as an additional active component. The composition and activity of the microbiome depend on physicochemical parameters such as sugar profile, pH, and water activity, which reflect the origin and authenticity of honey. Microorganisms present in honey produce metabolites with health-promoting properties, including antibacterial properties, which are a potential source of therapeutic compounds. Current methods for assessing honey quality rely primarily on chemical and microbiological analyses. An increasingly important role is played by advanced chromatographic techniques, which, when combined with chemometric tools, machine learning, and multi-omics, enable more precise and comprehensive evaluation of honey authenticity and quality. However, there are no standardized protocols integrating physicochemical, microbiological, and metabolomic data, which limits the full assessment of honey's bioactive potential. Future research should consider an integrated approach, combining traditional analytical methods with modern techniques, including omics and computational tools, to enable rapid and comprehensive assessment of the microbiome and its metabolites. This will allow the identification of bioactive compounds with therapeutic potential, while supporting authenticity verification, honey quality control, and bee health protection. This study focuses on a critical assessment of knowledge about the honey microbiome, its metabolites, and methods for studying them, identifying key research gaps and directions for future research. Important aspect is the correlation between honey microbiome and its properties.
Additional Links: PMID-41723992
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@article {pmid41723992,
year = {2026},
author = {Błońska, D and Szumski, M and Buszewski, B},
title = {Honey microbiome as a source of bioactive metabolites: the role of the microorganisms and the influence of physicochemical parameters.},
journal = {Journal of chromatography. A},
volume = {1772},
number = {},
pages = {466820},
doi = {10.1016/j.chroma.2026.466820},
pmid = {41723992},
issn = {1873-3778},
abstract = {Beyond its nutritional and therapeutic properties, honey contains a unique microbiome that may also function as an additional active component. The composition and activity of the microbiome depend on physicochemical parameters such as sugar profile, pH, and water activity, which reflect the origin and authenticity of honey. Microorganisms present in honey produce metabolites with health-promoting properties, including antibacterial properties, which are a potential source of therapeutic compounds. Current methods for assessing honey quality rely primarily on chemical and microbiological analyses. An increasingly important role is played by advanced chromatographic techniques, which, when combined with chemometric tools, machine learning, and multi-omics, enable more precise and comprehensive evaluation of honey authenticity and quality. However, there are no standardized protocols integrating physicochemical, microbiological, and metabolomic data, which limits the full assessment of honey's bioactive potential. Future research should consider an integrated approach, combining traditional analytical methods with modern techniques, including omics and computational tools, to enable rapid and comprehensive assessment of the microbiome and its metabolites. This will allow the identification of bioactive compounds with therapeutic potential, while supporting authenticity verification, honey quality control, and bee health protection. This study focuses on a critical assessment of knowledge about the honey microbiome, its metabolites, and methods for studying them, identifying key research gaps and directions for future research. Important aspect is the correlation between honey microbiome and its properties.},
}
RevDate: 2026-02-21
CmpDate: 2026-02-22
Alcohol consumption in metabolic dysfunction-associated steatotic liver disease (MASLD): understanding the gut-liver crosstalk for clinical translation.
Gut microbes, 18(1):2631834.
OBJECTIVE: In the present study, we investigated the role of the gut-liver crosstalk in the pathogenesis of steatotic liver disease (SLD) induced by the compounding and deleterious effects of alcohol and metabolic risk factors, and explored the potential translational aspects of microbiome-based interventions.
DESIGN: The effects of combined exposure to alcohol and a high-fat, high-cholesterol diet (HFHC) Western diet (WD) were tested in a dietary mouse DUAL model and compared to mice fed only with WD. Liver and gut phenotypes were evaluated via histochemistry, flow cytometry, gene expression, proteomic, and metabolomic analyses. The effects on the gut microbiota were studied in both DUAL mice and MASLD patients with a history of alcohol consumption. Antibiotic-induced microbiota depletion (AIMD) and microbiota modulation therapies (probiotics and fecal microbiota transplant (FMT)) were performed in mice. Primary human hepatocytes and HepG2 cells were used to study the underlying mechanisms. Zebrafish larvae exposed to alcohol and a HFHC diet were used as a validation model.
RESULTS: Alcohol in combination with WD synergistically exacerbated SLD. DUAL-diet-induced disruption of the intestinal barrier led to LPS leakage into the bloodstream and subsequent TLR4-mediated hepatic inflammation. This, together with enhanced intestinal fat absorption, and impaired intrahepatic lipid oxidation - particularly due to insufficient CPT-1 activity - contributed to prominent steatohepatitis. The DUAL-induced changes in the gut microbiota showed similarities to human dysbiosis in MASLD patients who consumed alcohol, including an increase in Bacteroides and Alistipes. AIMD improved pathology, indicating a causal role of the microbiota in the pathophysiology of DUAL steatohepatitis, whilst early microbiome modulation via FMT induced mild improvements in liver and gut physiology.
CONCLUSIONS: These results indicated that the microbiota‒gut‒liver axis plays a crucial role in the progression of SLD intensified by alcohol and concurrent metabolic risk factors, thus providing a promising translational target for potential therapeutic interventions.
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@article {pmid41723574,
year = {2026},
author = {Benedé-Ubieto, R and Estévez-Vázquez, O and Acar, R and Leal-Lassalle, H and Gutierrez, AH and Redondo-Urzainqui, A and Iborra, S and Odintsova, VE and Tyakht, A and Herranz, JM and Firat, Z and Basol, M and Korkmaz, B and Sanz-García, C and Juanola, O and Caparrós, E and Francés, R and Ciudin, A and Pericàs, JM and Gómez-Santos, B and Aspichueta, P and Treichel, N and Clavel, T and Reißing, J and Bruns, T and Bartneck, M and Mazariegos, MS and Wolters, JC and Jorquera, G and Liedtke, C and Vaquero, J and Bañares, R and Cakan-Akdogan, G and Ávila, MA and Konu, O and Cubero, FJ and Nevzorova, YA},
title = {Alcohol consumption in metabolic dysfunction-associated steatotic liver disease (MASLD): understanding the gut-liver crosstalk for clinical translation.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2631834},
pmid = {41723574},
issn = {1949-0984},
mesh = {Animals ; Humans ; *Gastrointestinal Microbiome/drug effects ; Mice ; Male ; *Liver/metabolism/pathology/drug effects ; Disease Models, Animal ; *Alcohol Drinking/adverse effects ; Zebrafish ; Mice, Inbred C57BL ; Diet, High-Fat/adverse effects ; *Fatty Liver/microbiology/metabolism/etiology ; Hep G2 Cells ; Fecal Microbiota Transplantation ; Female ; Diet, Western/adverse effects ; Hepatocytes/metabolism ; Dysbiosis ; Middle Aged ; },
abstract = {OBJECTIVE: In the present study, we investigated the role of the gut-liver crosstalk in the pathogenesis of steatotic liver disease (SLD) induced by the compounding and deleterious effects of alcohol and metabolic risk factors, and explored the potential translational aspects of microbiome-based interventions.
DESIGN: The effects of combined exposure to alcohol and a high-fat, high-cholesterol diet (HFHC) Western diet (WD) were tested in a dietary mouse DUAL model and compared to mice fed only with WD. Liver and gut phenotypes were evaluated via histochemistry, flow cytometry, gene expression, proteomic, and metabolomic analyses. The effects on the gut microbiota were studied in both DUAL mice and MASLD patients with a history of alcohol consumption. Antibiotic-induced microbiota depletion (AIMD) and microbiota modulation therapies (probiotics and fecal microbiota transplant (FMT)) were performed in mice. Primary human hepatocytes and HepG2 cells were used to study the underlying mechanisms. Zebrafish larvae exposed to alcohol and a HFHC diet were used as a validation model.
RESULTS: Alcohol in combination with WD synergistically exacerbated SLD. DUAL-diet-induced disruption of the intestinal barrier led to LPS leakage into the bloodstream and subsequent TLR4-mediated hepatic inflammation. This, together with enhanced intestinal fat absorption, and impaired intrahepatic lipid oxidation - particularly due to insufficient CPT-1 activity - contributed to prominent steatohepatitis. The DUAL-induced changes in the gut microbiota showed similarities to human dysbiosis in MASLD patients who consumed alcohol, including an increase in Bacteroides and Alistipes. AIMD improved pathology, indicating a causal role of the microbiota in the pathophysiology of DUAL steatohepatitis, whilst early microbiome modulation via FMT induced mild improvements in liver and gut physiology.
CONCLUSIONS: These results indicated that the microbiota‒gut‒liver axis plays a crucial role in the progression of SLD intensified by alcohol and concurrent metabolic risk factors, thus providing a promising translational target for potential therapeutic interventions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Humans
*Gastrointestinal Microbiome/drug effects
Mice
Male
*Liver/metabolism/pathology/drug effects
Disease Models, Animal
*Alcohol Drinking/adverse effects
Zebrafish
Mice, Inbred C57BL
Diet, High-Fat/adverse effects
*Fatty Liver/microbiology/metabolism/etiology
Hep G2 Cells
Fecal Microbiota Transplantation
Female
Diet, Western/adverse effects
Hepatocytes/metabolism
Dysbiosis
Middle Aged
RevDate: 2026-02-21
Gut microbial signatures and immunotherapy outcomes in NSCLC and melanoma: a systematic review and meta-analysis.
BMC cancer pii:10.1186/s12885-026-15763-3 [Epub ahead of print].
Additional Links: PMID-41723389
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PubMed:
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@article {pmid41723389,
year = {2026},
author = {Essa, MEA and Noori, H and Butler, J and Ahmed, AA},
title = {Gut microbial signatures and immunotherapy outcomes in NSCLC and melanoma: a systematic review and meta-analysis.},
journal = {BMC cancer},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12885-026-15763-3},
pmid = {41723389},
issn = {1471-2407},
}
RevDate: 2026-02-21
Social disconnection: from cortisol-oxytocin imbalance to endothelial dysfunction, a narrative review of mechanisms and potential interventions.
Trends in cardiovascular medicine pii:S1050-1738(26)00029-0 [Epub ahead of print].
Social disconnection, both in the form of social isolation and loneliness, is increasingly recognized as a clinically significant but underappreciated risk factor for cardiovascular disease (CVD), affecting 16-25% of individuals. Population studies have consistently linked social disconnection to a higher risk of all-cause mortality, myocardial infarction, stroke, and cardiovascular death, yet routine screening for social disconnection is uncommon in everyday clinical practice. Even when identified, due to both lack of strong evidence-based interventions and awareness about them, meaningful clinical changes are seldom observed. In light of growing recognition by major health authorities, including the World Health Organization and the U.S. Surgeon General and of the Harvard Study of Adult Development, showing that social integration and strong relationships are the most powerful predictors of healthy aging, we conducted a narrative literature review synthesizing current evidence on the relationship between social disconnection and CVD. The mechanism mediating social disconnection and cardiovascular events is still a matter of debate. We focus on cortisol-oxytocin imbalance and highlight that it is central in causing CVD through autonomic dysregulation, nutritional imbalance and gut microbiome alterations. Alongside psychosocial comorbidities, these factors may converge on endothelial dysfunction as an initiating mechanism of CVD. Our review also aims to foster discussion on how to recognize and address social disconnection in clinical practice, emphasizing the need for structured, multidisciplinary pathways as well as trials assessing their effect on improving both social disconnection and the associated CVD risk.
Additional Links: PMID-41722663
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@article {pmid41722663,
year = {2026},
author = {Manzato, M and Hamidabad, NM and Clark, MM and Pardo, LS and Montone, RA and Lerman, LO and Lerman, A},
title = {Social disconnection: from cortisol-oxytocin imbalance to endothelial dysfunction, a narrative review of mechanisms and potential interventions.},
journal = {Trends in cardiovascular medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tcm.2026.01.007},
pmid = {41722663},
issn = {1873-2615},
abstract = {Social disconnection, both in the form of social isolation and loneliness, is increasingly recognized as a clinically significant but underappreciated risk factor for cardiovascular disease (CVD), affecting 16-25% of individuals. Population studies have consistently linked social disconnection to a higher risk of all-cause mortality, myocardial infarction, stroke, and cardiovascular death, yet routine screening for social disconnection is uncommon in everyday clinical practice. Even when identified, due to both lack of strong evidence-based interventions and awareness about them, meaningful clinical changes are seldom observed. In light of growing recognition by major health authorities, including the World Health Organization and the U.S. Surgeon General and of the Harvard Study of Adult Development, showing that social integration and strong relationships are the most powerful predictors of healthy aging, we conducted a narrative literature review synthesizing current evidence on the relationship between social disconnection and CVD. The mechanism mediating social disconnection and cardiovascular events is still a matter of debate. We focus on cortisol-oxytocin imbalance and highlight that it is central in causing CVD through autonomic dysregulation, nutritional imbalance and gut microbiome alterations. Alongside psychosocial comorbidities, these factors may converge on endothelial dysfunction as an initiating mechanism of CVD. Our review also aims to foster discussion on how to recognize and address social disconnection in clinical practice, emphasizing the need for structured, multidisciplinary pathways as well as trials assessing their effect on improving both social disconnection and the associated CVD risk.},
}
RevDate: 2026-02-21
Age-related sarcopenia and the gut microbiome: mechanistic insights into the gut-muscle axis and potential microbiome based therapeutic interventions.
Ageing research reviews pii:S1568-1637(26)00057-7 [Epub ahead of print].
Ageing is associated with a loss of skeletal muscle mass, strength and function, termed sarcopenia. The presence of sarcopenia is known to be problematic leading to an increased risk of falls, fractures and mortality. Age-related changes in the gut microbiome, characterized by reduced diversity and altered metabolite production, may compromise intestinal barrier function, leading to increased permeability. These age-associated changes in the gut microbiome led to changes in circulating microbial metabolites and toxins, such as a decrease in short-chain fatty acids, an increase in lipopolysaccharides and an imbalance in bile acid production. Together these alterations may contribute to the development of sarcopenia through impairments in muscle protein turnover. Currently, lifestyle-based approaches e.g., exercise and diet, alongside the use of pre-, pro- and post-biotics have been proposed as strategies to target the gut-muscle axis and combat the risk of sarcopenia in the expanding ageing population. However, little evidence is available to support their use within clinical settings. Several new strategies including the nutraceutical Urolithin A and faecal microbiome transplants (FMT) have been suggested to treat age-related sarcopenia. This review provides insight into the potential interactions of the gut microbiome and skeletal muscle with ageing and sarcopenia development, alongside potential new and existing countermeasures.
Additional Links: PMID-41722622
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@article {pmid41722622,
year = {2026},
author = {Allen, SL and Breen, L and Lord, JM and Duggal, NA},
title = {Age-related sarcopenia and the gut microbiome: mechanistic insights into the gut-muscle axis and potential microbiome based therapeutic interventions.},
journal = {Ageing research reviews},
volume = {},
number = {},
pages = {103065},
doi = {10.1016/j.arr.2026.103065},
pmid = {41722622},
issn = {1872-9649},
abstract = {Ageing is associated with a loss of skeletal muscle mass, strength and function, termed sarcopenia. The presence of sarcopenia is known to be problematic leading to an increased risk of falls, fractures and mortality. Age-related changes in the gut microbiome, characterized by reduced diversity and altered metabolite production, may compromise intestinal barrier function, leading to increased permeability. These age-associated changes in the gut microbiome led to changes in circulating microbial metabolites and toxins, such as a decrease in short-chain fatty acids, an increase in lipopolysaccharides and an imbalance in bile acid production. Together these alterations may contribute to the development of sarcopenia through impairments in muscle protein turnover. Currently, lifestyle-based approaches e.g., exercise and diet, alongside the use of pre-, pro- and post-biotics have been proposed as strategies to target the gut-muscle axis and combat the risk of sarcopenia in the expanding ageing population. However, little evidence is available to support their use within clinical settings. Several new strategies including the nutraceutical Urolithin A and faecal microbiome transplants (FMT) have been suggested to treat age-related sarcopenia. This review provides insight into the potential interactions of the gut microbiome and skeletal muscle with ageing and sarcopenia development, alongside potential new and existing countermeasures.},
}
RevDate: 2026-02-21
Identifying microbial protease allergens through protein language model-guided homology.
Cell systems pii:S2405-4712(25)00343-6 [Epub ahead of print].
Emerging research links the gut, skin, and oral microbiomes to allergies, with serine proteases (SPs) identified as potential allergens. This study leverages deep learning and pre-trained protein language models (pLMs) to uncover allergenic SPs in metagenomic data. First, we develop a model to identify the catalytic serine residue in serine hydrolases, demonstrating how pLMs capture structural information. Next, we create a deep learning framework to detect candidate SP allergens across gene catalogs, using the conserved catalytic triad to identify homologs in gut and oral sites despite low sequence identity. Our model predicts a putative SP allergen resembling V8 protease, a known trigger for protease-activated receptor 1. It also identifies a cysteine protease similar to Der f 1 from dust mites. Immunization with these proteases induced allergic responses, validating their allergenic potential experimentally. This approach uncovers candidate allergens beyond traditional methods, offering new targets for allergy research. A record of this paper's transparent peer review process is included in the supplemental information.
Additional Links: PMID-41722567
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@article {pmid41722567,
year = {2026},
author = {Thurimella, K and Wu, E and Li, C and Graham, DB and Owens, RM and Plichta, DR and Sokol, CL and Xavier, RJ and Bacallado, S},
title = {Identifying microbial protease allergens through protein language model-guided homology.},
journal = {Cell systems},
volume = {},
number = {},
pages = {101510},
doi = {10.1016/j.cels.2025.101510},
pmid = {41722567},
issn = {2405-4720},
abstract = {Emerging research links the gut, skin, and oral microbiomes to allergies, with serine proteases (SPs) identified as potential allergens. This study leverages deep learning and pre-trained protein language models (pLMs) to uncover allergenic SPs in metagenomic data. First, we develop a model to identify the catalytic serine residue in serine hydrolases, demonstrating how pLMs capture structural information. Next, we create a deep learning framework to detect candidate SP allergens across gene catalogs, using the conserved catalytic triad to identify homologs in gut and oral sites despite low sequence identity. Our model predicts a putative SP allergen resembling V8 protease, a known trigger for protease-activated receptor 1. It also identifies a cysteine protease similar to Der f 1 from dust mites. Immunization with these proteases induced allergic responses, validating their allergenic potential experimentally. This approach uncovers candidate allergens beyond traditional methods, offering new targets for allergy research. A record of this paper's transparent peer review process is included in the supplemental information.},
}
RevDate: 2026-02-21
Probiotic therapeutics: A critical review of mechanisms, clinical efficacy, and the frontier of precision microbiome modulation.
International immunopharmacology, 175:116412 pii:S1567-5769(26)00256-0 [Epub ahead of print].
Probiotic therapeutics are evolving from generalized wellness supplements to precision Live Biotherapeutic Products aimed at specific disease targets. This review elucidates the multi-layered mechanistic framework of probiotic action, which spans ecological niche modulation, epithelial barrier reinforcement, and systemic signaling via the gut-brain axis. While clinical efficacy is established for conditions like antibiotic-associated diarrhea, trial outcomes remain highly heterogeneous for complex disorders such as irritable bowel syndrome and metabolic syndrome. We deconstruct this variability, attributing it to critical factors often overlooked in study design: stringent strain-specificity, host-specific colonization resistance, and the lack of standardized core outcome sets. The field is now advancing toward precision microbiome modulation through next-generation biotics like Akkermansia muciniphila, synbiotics, and engineered microbial therapeutics. We conclude that integrating multi-omics technologies with artificial intelligence is essential to transition from empirical supplementation to personalized, evidence-based clinical practice.
Additional Links: PMID-41722541
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@article {pmid41722541,
year = {2026},
author = {Ashaolu, TJ and Suttikhana, I},
title = {Probiotic therapeutics: A critical review of mechanisms, clinical efficacy, and the frontier of precision microbiome modulation.},
journal = {International immunopharmacology},
volume = {175},
number = {},
pages = {116412},
doi = {10.1016/j.intimp.2026.116412},
pmid = {41722541},
issn = {1878-1705},
abstract = {Probiotic therapeutics are evolving from generalized wellness supplements to precision Live Biotherapeutic Products aimed at specific disease targets. This review elucidates the multi-layered mechanistic framework of probiotic action, which spans ecological niche modulation, epithelial barrier reinforcement, and systemic signaling via the gut-brain axis. While clinical efficacy is established for conditions like antibiotic-associated diarrhea, trial outcomes remain highly heterogeneous for complex disorders such as irritable bowel syndrome and metabolic syndrome. We deconstruct this variability, attributing it to critical factors often overlooked in study design: stringent strain-specificity, host-specific colonization resistance, and the lack of standardized core outcome sets. The field is now advancing toward precision microbiome modulation through next-generation biotics like Akkermansia muciniphila, synbiotics, and engineered microbial therapeutics. We conclude that integrating multi-omics technologies with artificial intelligence is essential to transition from empirical supplementation to personalized, evidence-based clinical practice.},
}
RevDate: 2026-02-21
Mechanistic insights into cordycepin-enhanced CTLA-4 blockade efficacy via Eubacterium rectale-mediated immunomodulation in colon cancer.
International immunopharmacology, 175:116406 pii:S1567-5769(26)00250-X [Epub ahead of print].
Colon cancer remains a therapeutic challenge due to limited efficacy of current treatments. This study investigates the synergistic antitumor effects of cordycepin combined with CTLA-4 inhibitors, focusing on their ability to reshape the gut microbiome. By integrating multi-omics approaches, we elucidate the mechanisms underlying the enhanced efficacy of this triple therapy. Our findings reveal that cordycepin combined with CTLA-4 inhibitors significantly improves antitumor efficacy in the MC38 colon cancer mouse model. This enhancement is mediated by the critical role of the Eubacterium brachy group in modulating the tumor immune microenvironment. Based on these results, we propose a "microbiome-immune" triple therapy strategy involving cordycepin, CTLA-4 inhibitors, and Eubacterium rectale. Non-targeted metabolomics analysis using LC-MS identified specific activation of the histidine metabolism pathway, with elevated levels of the key metabolite Cetirizine N-Oxide potentially contributing to enhanced immune activity. Single-cell transcriptomic analysis demonstrated that the triple therapy significantly increased the responsiveness of tumor antigen-specific CD8[+] T cells to CTLA-4 inhibitors, thereby boosting their antitumor activity. Moreover, the triple therapy not only enhanced the antitumor functionality of conventional effector CD4[+] T cells but also effectively prevented their exhaustion. Mechanistic studies further revealed that the triple therapy suppresses the activity of the Bcl6 regulatory network, thereby reducing the immunosuppressive function of Tregs and destroying the immunosuppressive interplay between myeloid immune cells and Tregs. These results demonstrate a promising "microbiome-immune" dual-targeting strategy for colon cancer with clinical translational potential.
Additional Links: PMID-41722537
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@article {pmid41722537,
year = {2026},
author = {Gao, X and Feng, C and Deng, Y and Chen, R and Wu, H and Wu, S and Yang, J and Xu, Q and Hu, N and Zhang, W and Chen, L and Zheng, X and Tang, C and Jiang, J},
title = {Mechanistic insights into cordycepin-enhanced CTLA-4 blockade efficacy via Eubacterium rectale-mediated immunomodulation in colon cancer.},
journal = {International immunopharmacology},
volume = {175},
number = {},
pages = {116406},
doi = {10.1016/j.intimp.2026.116406},
pmid = {41722537},
issn = {1878-1705},
abstract = {Colon cancer remains a therapeutic challenge due to limited efficacy of current treatments. This study investigates the synergistic antitumor effects of cordycepin combined with CTLA-4 inhibitors, focusing on their ability to reshape the gut microbiome. By integrating multi-omics approaches, we elucidate the mechanisms underlying the enhanced efficacy of this triple therapy. Our findings reveal that cordycepin combined with CTLA-4 inhibitors significantly improves antitumor efficacy in the MC38 colon cancer mouse model. This enhancement is mediated by the critical role of the Eubacterium brachy group in modulating the tumor immune microenvironment. Based on these results, we propose a "microbiome-immune" triple therapy strategy involving cordycepin, CTLA-4 inhibitors, and Eubacterium rectale. Non-targeted metabolomics analysis using LC-MS identified specific activation of the histidine metabolism pathway, with elevated levels of the key metabolite Cetirizine N-Oxide potentially contributing to enhanced immune activity. Single-cell transcriptomic analysis demonstrated that the triple therapy significantly increased the responsiveness of tumor antigen-specific CD8[+] T cells to CTLA-4 inhibitors, thereby boosting their antitumor activity. Moreover, the triple therapy not only enhanced the antitumor functionality of conventional effector CD4[+] T cells but also effectively prevented their exhaustion. Mechanistic studies further revealed that the triple therapy suppresses the activity of the Bcl6 regulatory network, thereby reducing the immunosuppressive function of Tregs and destroying the immunosuppressive interplay between myeloid immune cells and Tregs. These results demonstrate a promising "microbiome-immune" dual-targeting strategy for colon cancer with clinical translational potential.},
}
RevDate: 2026-02-21
Comprehensive analysis of spoilage characteristics of refrigerated hairtail by microbiome and metabolomics.
International journal of food microbiology, 452:111671 pii:S0168-1605(26)00051-6 [Epub ahead of print].
Hairtail is prone to spoilage during refrigerated storage and it is due to microbial activity, which will directly lead to changes in the composition of metabolites in vivo. This study systematically elucidates the spoilage phenomena in hairtail during eight days of refrigeration at 4 °C through multi-omics analysis. Pseudomonas and Shewanella were identified as key spoilage bacteria, and their nutrient utilization pathways were different Pseudomonas dominated the early stage and used monosaccharides; however, Shewanella appeared in the later stage, and its metabolism is heavily dependent on amino acids and nitrogen-containing compounds such as TMAO released in large quantities in the later stage of spoilage. Non-targeted metabolomics results revealed a total of 62 differentially expressed metabolites. Metabolic pathway enrichment analysis revealed that cysteine and methionine metabolism, tyrosine metabolism and nucleotide metabolism played pivotal roles in the putrefaction process. Moreover, the study identified 7 metabolites (such as Lys-Met, Nicotinic Acid Adenine Dinucleotide) that showed a significant correlation with the dominant spoilage bacterium Pseudomonas through correlation analysis; while two other metabolites (such as Inosine 5'-Monophosphate, Tyramine) were significantly correlated with the primary spoilage bacterium Shewanella. The integration of microbiome and metabolomics analyses has enabled the precise identification of key spoilage microorganisms and metabolites in chilled hairtail, providing crucial evidence for developing targeted preservation techniques.
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@article {pmid41722523,
year = {2026},
author = {Wang, H and Zhang, W and Chen, M and Wang, J and Liu, X and Guo, X and Zhang, B and Deng, S and Tang, M and Chen, J},
title = {Comprehensive analysis of spoilage characteristics of refrigerated hairtail by microbiome and metabolomics.},
journal = {International journal of food microbiology},
volume = {452},
number = {},
pages = {111671},
doi = {10.1016/j.ijfoodmicro.2026.111671},
pmid = {41722523},
issn = {1879-3460},
abstract = {Hairtail is prone to spoilage during refrigerated storage and it is due to microbial activity, which will directly lead to changes in the composition of metabolites in vivo. This study systematically elucidates the spoilage phenomena in hairtail during eight days of refrigeration at 4 °C through multi-omics analysis. Pseudomonas and Shewanella were identified as key spoilage bacteria, and their nutrient utilization pathways were different Pseudomonas dominated the early stage and used monosaccharides; however, Shewanella appeared in the later stage, and its metabolism is heavily dependent on amino acids and nitrogen-containing compounds such as TMAO released in large quantities in the later stage of spoilage. Non-targeted metabolomics results revealed a total of 62 differentially expressed metabolites. Metabolic pathway enrichment analysis revealed that cysteine and methionine metabolism, tyrosine metabolism and nucleotide metabolism played pivotal roles in the putrefaction process. Moreover, the study identified 7 metabolites (such as Lys-Met, Nicotinic Acid Adenine Dinucleotide) that showed a significant correlation with the dominant spoilage bacterium Pseudomonas through correlation analysis; while two other metabolites (such as Inosine 5'-Monophosphate, Tyramine) were significantly correlated with the primary spoilage bacterium Shewanella. The integration of microbiome and metabolomics analyses has enabled the precise identification of key spoilage microorganisms and metabolites in chilled hairtail, providing crucial evidence for developing targeted preservation techniques.},
}
RevDate: 2026-02-23
Correction to: Function-based selection of synthetic communities enables mechanistic microbiome studies.
The ISME journal, 20(1):.
Additional Links: PMID-41722097
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@article {pmid41722097,
year = {2026},
author = {},
title = {Correction to: Function-based selection of synthetic communities enables mechanistic microbiome studies.},
journal = {The ISME journal},
volume = {20},
number = {1},
pages = {},
doi = {10.1093/ismejo/wrag015},
pmid = {41722097},
issn = {1751-7370},
}
RevDate: 2026-02-21
No systematic difference in obesity susceptibility between two groups of zoo primates with distinct digestive physiologies: hindgut-fermenting lemurs and foregut-fermenting colobines.
Primates; journal of primatology [Epub ahead of print].
Obesity is an often-stated issue in zoo animals, including primates, and has historically been particularly emphasized for lemurs. By contrast, similar reports for colobine species-which are literally called 'slim monkeys' in at least one other language-are absent. This has been hypothsized to be linked to the colobine foregut fermentation system; diets high in easily digestible carbohydrates might disturb the microbiome in the foregut, similar to acidosis in domestic ruminants, leading to reduced intake and disease rather than obesity, but empirical data is lacking. We compared body mass (BM) data for 14 lemur species (7187 individuals) and 10 colobine species (1443 individuals) with literature data on free-ranging specimens to test this concept. In contrast to expectations, a similar percentage of species had a majority of individuals above the 'healthy' BM range in at least one sex (36% of lemur and 40% of colobine species). However, colobines had a higher percentage of individuals considered 'underweight', especially in the two rarely kept species with the more complex 'quadripartite' stomachs (Nasalis larvatus, Pygathrix nemaeus). Neither sample size, sexual size dimorphism, the degree of folivory, nor indications for a seasonal physiology were clearly associated with species' propensity for zoo obesity. There were no clear historical trends in the development of obesity in these species. We conclude that no general rules about species' susceptibility to obesity appear to apply. Body mass and condition of zoo primates should be monitored continuously, and feeding regimes possibly be adapted to contain diets of higher fibre levels more similar to those reported in natural diets.
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@article {pmid41721948,
year = {2026},
author = {Krauss, C and Garand, E and Hahn-Klimroth, M and Müller, DWH and Dierkes, PW and Matsuda, I and Clauss, M and Meireles, JP},
title = {No systematic difference in obesity susceptibility between two groups of zoo primates with distinct digestive physiologies: hindgut-fermenting lemurs and foregut-fermenting colobines.},
journal = {Primates; journal of primatology},
volume = {},
number = {},
pages = {},
pmid = {41721948},
issn = {1610-7365},
support = {(#25K22873, #23K27254 and #19KK0191//JSPS KAKENHI/ ; },
abstract = {Obesity is an often-stated issue in zoo animals, including primates, and has historically been particularly emphasized for lemurs. By contrast, similar reports for colobine species-which are literally called 'slim monkeys' in at least one other language-are absent. This has been hypothsized to be linked to the colobine foregut fermentation system; diets high in easily digestible carbohydrates might disturb the microbiome in the foregut, similar to acidosis in domestic ruminants, leading to reduced intake and disease rather than obesity, but empirical data is lacking. We compared body mass (BM) data for 14 lemur species (7187 individuals) and 10 colobine species (1443 individuals) with literature data on free-ranging specimens to test this concept. In contrast to expectations, a similar percentage of species had a majority of individuals above the 'healthy' BM range in at least one sex (36% of lemur and 40% of colobine species). However, colobines had a higher percentage of individuals considered 'underweight', especially in the two rarely kept species with the more complex 'quadripartite' stomachs (Nasalis larvatus, Pygathrix nemaeus). Neither sample size, sexual size dimorphism, the degree of folivory, nor indications for a seasonal physiology were clearly associated with species' propensity for zoo obesity. There were no clear historical trends in the development of obesity in these species. We conclude that no general rules about species' susceptibility to obesity appear to apply. Body mass and condition of zoo primates should be monitored continuously, and feeding regimes possibly be adapted to contain diets of higher fibre levels more similar to those reported in natural diets.},
}
RevDate: 2026-02-21
From Rodents to Chips: Preclinical Models of Inflammatory Bowel Disease with Emphasis on Host-Microbiome Interactions.
American journal of physiology. Gastrointestinal and liver physiology [Epub ahead of print].
Inflammatory bowel disease (IBD), comprising Crohn's disease and ulcerative colitis, is a chronic relapsing inflammatory disorder with steadily increasing global prevalence, significantly impairing patient quality of life. Preclinical research in IBD has traditionally relied on animal models to investigate disease etiology, immunopathogenesis, and therapeutic responses. A wide range of experimental models primarily rodents, along with limited use of larger animals such as pigs and non-human primates-have been developed to reproduce key clinical, histological, and immunological features of human IBD. These models have played a crucial role in evaluating pharmacological agents, biologics, probiotics, dietary interventions, gene-based therapies, and microbiome-targeted strategies. Notably, accumulating evidence highlights the pivotal role of gut microbiota dysbiosis in disease initiation, progression, and therapeutic responsiveness, making host-microbiome interactions a central component of contemporary IBD research. However, despite their utility, animal models exhibit important limitations related to interspecies differences, incomplete microbiome representation, and poor translational predictability. In response, increasing regulatory pressure from agencies such as the NIH and FDA to reduce animal experimentation has accelerated the development of human-relevant, non-animal platforms, including intestinal organoids, 3D in vitro co-culture systems, and gut-on-chip technologies. This review critically evaluates existing in vivo IBD models with particular emphasis on their ability to capture immune-microbiome epithelial interactions, while also discussing emerging human-derived systems as complementary translational tools. Collectively, the integration of microbiome-responsive and immune-competent advanced in vitro models represents a promising direction to bridge the gap between experimental findings and clinical application in IBD research.
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@article {pmid41721794,
year = {2026},
author = {Kumar, S and Sarkar, B},
title = {From Rodents to Chips: Preclinical Models of Inflammatory Bowel Disease with Emphasis on Host-Microbiome Interactions.},
journal = {American journal of physiology. Gastrointestinal and liver physiology},
volume = {},
number = {},
pages = {},
doi = {10.1152/ajpgi.00345.2025},
pmid = {41721794},
issn = {1522-1547},
support = {APO/PhD/IRS/2024-25/26//Birla Institute of Technology and Science, Mesra (BITS Mesra)/ ; },
abstract = {Inflammatory bowel disease (IBD), comprising Crohn's disease and ulcerative colitis, is a chronic relapsing inflammatory disorder with steadily increasing global prevalence, significantly impairing patient quality of life. Preclinical research in IBD has traditionally relied on animal models to investigate disease etiology, immunopathogenesis, and therapeutic responses. A wide range of experimental models primarily rodents, along with limited use of larger animals such as pigs and non-human primates-have been developed to reproduce key clinical, histological, and immunological features of human IBD. These models have played a crucial role in evaluating pharmacological agents, biologics, probiotics, dietary interventions, gene-based therapies, and microbiome-targeted strategies. Notably, accumulating evidence highlights the pivotal role of gut microbiota dysbiosis in disease initiation, progression, and therapeutic responsiveness, making host-microbiome interactions a central component of contemporary IBD research. However, despite their utility, animal models exhibit important limitations related to interspecies differences, incomplete microbiome representation, and poor translational predictability. In response, increasing regulatory pressure from agencies such as the NIH and FDA to reduce animal experimentation has accelerated the development of human-relevant, non-animal platforms, including intestinal organoids, 3D in vitro co-culture systems, and gut-on-chip technologies. This review critically evaluates existing in vivo IBD models with particular emphasis on their ability to capture immune-microbiome epithelial interactions, while also discussing emerging human-derived systems as complementary translational tools. Collectively, the integration of microbiome-responsive and immune-competent advanced in vitro models represents a promising direction to bridge the gap between experimental findings and clinical application in IBD research.},
}
RevDate: 2026-02-21
Dysbiosis in the Pathogenesis of Atopic Dermatitis.
The Journal of dermatology [Epub ahead of print].
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by epidermal barrier dysfunction and immune dysregulation. Recent research highlights cutaneous dysbiosis as a critical factor in its pathogenesis. In this review, we summarize the interplay between the skin microbiota and host immunity, contrasting the homeostatic state with the dysbiosis in AD. In healthy skin, resident microbial communities, including coagulase-negative staphylococci and Cutibacterium acnes, contribute to immune education and pathogen defense. In AD, this equilibrium is disrupted, leading to a state of functional dysbiosis characterized not only by reduced microbial diversity and the predominance of Staphylococcus aureus but also by the loss of protective commensal functions. The virulence of S. aureus is pivotal, with its accessory gene regulator (Agr) quorum-sensing system driving the expression of toxins like δ-toxin, which exacerbates type 2 inflammation and barrier defects. Crucially, colonization in early life with S. aureus strains possessing a functional Agr system is strongly associated with an increased risk of subsequent AD development. This understanding has prompted a paradigm shift in therapeutic strategies. Recognizing the limitations of traditional broad-spectrum antimicrobials, which can worsen dysbiosis, novel approaches now focus on restoring microbial balance. These include bacteriotherapy using beneficial commensal strains to competitively inhibit S. aureus, quorum-quenching agents, and preventive skincare interventions initiated in infancy to foster a healthy microbiome. A deeper comprehension of these host-microbe and microbe-microbe interactions is essential for optimizing these promising microbiome-targeted therapies for AD.
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@article {pmid41721459,
year = {2026},
author = {Okamoto, H and Nakamura, Y},
title = {Dysbiosis in the Pathogenesis of Atopic Dermatitis.},
journal = {The Journal of dermatology},
volume = {},
number = {},
pages = {},
doi = {10.1111/1346-8138.70191},
pmid = {41721459},
issn = {1346-8138},
support = {KAKENHI 23K27621//Japan Society for the Promotion of Science/ ; JPMJFR200Y//JST FOREST/ ; 23gm1610004h0003//AMED-CREST/ ; 23ek0410105s0101//Japan Agency for Medical Research and Development/ ; //LEO Foundation award/ ; },
abstract = {Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by epidermal barrier dysfunction and immune dysregulation. Recent research highlights cutaneous dysbiosis as a critical factor in its pathogenesis. In this review, we summarize the interplay between the skin microbiota and host immunity, contrasting the homeostatic state with the dysbiosis in AD. In healthy skin, resident microbial communities, including coagulase-negative staphylococci and Cutibacterium acnes, contribute to immune education and pathogen defense. In AD, this equilibrium is disrupted, leading to a state of functional dysbiosis characterized not only by reduced microbial diversity and the predominance of Staphylococcus aureus but also by the loss of protective commensal functions. The virulence of S. aureus is pivotal, with its accessory gene regulator (Agr) quorum-sensing system driving the expression of toxins like δ-toxin, which exacerbates type 2 inflammation and barrier defects. Crucially, colonization in early life with S. aureus strains possessing a functional Agr system is strongly associated with an increased risk of subsequent AD development. This understanding has prompted a paradigm shift in therapeutic strategies. Recognizing the limitations of traditional broad-spectrum antimicrobials, which can worsen dysbiosis, novel approaches now focus on restoring microbial balance. These include bacteriotherapy using beneficial commensal strains to competitively inhibit S. aureus, quorum-quenching agents, and preventive skincare interventions initiated in infancy to foster a healthy microbiome. A deeper comprehension of these host-microbe and microbe-microbe interactions is essential for optimizing these promising microbiome-targeted therapies for AD.},
}
RevDate: 2026-02-20
Modulation of gut-heart axis by synbiotic (Lactiplantibacillus plantarum M10 and Isomaltose) in high cholesterol diet induced atherosclerotic murine model.
BMC microbiology pii:10.1186/s12866-026-04840-z [Epub ahead of print].
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@article {pmid41721244,
year = {2026},
author = {Patial, S and Raj, K and Shukla, G},
title = {Modulation of gut-heart axis by synbiotic (Lactiplantibacillus plantarum M10 and Isomaltose) in high cholesterol diet induced atherosclerotic murine model.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-04840-z},
pmid = {41721244},
issn = {1471-2180},
}
RevDate: 2026-02-20
Strain-level heterogeneity in Gardnerella urinary tract persistence and pathogenesis in an in vivo model is consistent with comparative phylogenomic analyses.
BMC microbiology pii:10.1186/s12866-026-04838-7 [Epub ahead of print].
Additional Links: PMID-41721237
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@article {pmid41721237,
year = {2026},
author = {Kumar, L and Whang, SN and Verges, DK and Potter, RF and Gilbert, NM},
title = {Strain-level heterogeneity in Gardnerella urinary tract persistence and pathogenesis in an in vivo model is consistent with comparative phylogenomic analyses.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-04838-7},
pmid = {41721237},
issn = {1471-2180},
support = {DK137964/DK/NIDDK NIH HHS/United States ; },
}
RevDate: 2026-02-20
Association between castration-induced changes in circadian body temperature rhythms and gut microbiome diversity in goats.
Scientific reports pii:10.1038/s41598-026-40455-0 [Epub ahead of print].
Castration is a routine management practice in livestock production, used to control temperament, reproduction, and carcass traits. Beyond these intended outcomes, castration induces substantial physiological changes, particularly in energy metabolism and thermoregulation. Recent studies have revealed close interactions between host circadian physiology and the gut microbiome, suggesting that disturbances in this relationship may influence animal performance and welfare. However, the effects of castration-induced alterations in circadian body temperature (CBT) rhythms on intestinal microbial composition remain poorly understood in ruminants. This study investigated the association between castration, CBT rhythmicity, and gut microbiota composition in goats. Castration significantly modified CBT rhythms in both early- and late-castrated animals. Linear mixed-effects cosinor analysis demonstrated distinct changes in the amplitude and acrophase of CBT oscillations, with more pronounced effects observed in late-castrated goats. These physiological changes were accompanied by shifts in intestinal microbial β-diversity, as shown by distance-based redundancy analysis, suggesting that castration-induced alterations in host circadian regulation were associated with changes in microbial community structure. Given the small sample size, this study should be considered exploratory and hypothesis-generating. These findings provide new insights into the interplay between host circadian biology and the gut microbiome in ruminants. The present study may inform future research and management approaches aimed at improving animal health and productivity.
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@article {pmid41720994,
year = {2026},
author = {Matsufuji, I and Kitagawa, Y and Ohkura, S and Morita, Y},
title = {Association between castration-induced changes in circadian body temperature rhythms and gut microbiome diversity in goats.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-40455-0},
pmid = {41720994},
issn = {2045-2322},
support = {JPMJSC24A2//Japan Science and Technology Agency/ ; 20K15647 and 24K09209//Japan Society for the Promotion of Science/ ; },
abstract = {Castration is a routine management practice in livestock production, used to control temperament, reproduction, and carcass traits. Beyond these intended outcomes, castration induces substantial physiological changes, particularly in energy metabolism and thermoregulation. Recent studies have revealed close interactions between host circadian physiology and the gut microbiome, suggesting that disturbances in this relationship may influence animal performance and welfare. However, the effects of castration-induced alterations in circadian body temperature (CBT) rhythms on intestinal microbial composition remain poorly understood in ruminants. This study investigated the association between castration, CBT rhythmicity, and gut microbiota composition in goats. Castration significantly modified CBT rhythms in both early- and late-castrated animals. Linear mixed-effects cosinor analysis demonstrated distinct changes in the amplitude and acrophase of CBT oscillations, with more pronounced effects observed in late-castrated goats. These physiological changes were accompanied by shifts in intestinal microbial β-diversity, as shown by distance-based redundancy analysis, suggesting that castration-induced alterations in host circadian regulation were associated with changes in microbial community structure. Given the small sample size, this study should be considered exploratory and hypothesis-generating. These findings provide new insights into the interplay between host circadian biology and the gut microbiome in ruminants. The present study may inform future research and management approaches aimed at improving animal health and productivity.},
}
RevDate: 2026-02-20
Developmental plasticity enables an intestinal tapeworm to adapt to dietary stress.
Nature communications pii:10.1038/s41467-026-69475-0 [Epub ahead of print].
Diet is one of the strongest ecological forces shaping the gut environment, yet its impact on intestinal worms (helminths) remains poorly understood. The helminth Hymenolepis diminuta is a suitable model for investigating how lifestyle changes in modern societies may disrupt host-helminth relationships. Here we show that dietary fiber availability shapes the developmental trajectory and life strategies of H. diminuta in a stage-dependent manner. Fiber deprivation at the time of host colonization leads to developmental arrest, manifested by reduced growth, absence of reproduction, and transcriptional changes consistent with suppressed development. This state is accompanied by diet-dependent remodeling of the host small intestinal microbiota and metabolome: whereas fiber-rich diets support fermentative microbial communities and a chemically diverse intestinal environment, the Western diet promotes dysbiotic profiles with reduced fermentation capacity and a more pro-inflammatory immune response. In contrast, adult H. diminuta that reach maturity in hosts maintained on a fiber-rich diet exhibit a reversible, estivation-like suppression of reproduction during short-term fiber deprivation, with full restoration of egg production following dietary recovery. Together, these findings indicate that dietary transitions associated with industrialized lifestyles can redirect helminth developmental programs and host-helminth-microbiome interactions, with implications for helminth persistence and potential therapeutic applications.
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@article {pmid41720781,
year = {2026},
author = {Jirků, M and Parker, W and Kadlecová, O and Moos, M and Wiśniewska, MM and Kuchta, R and Tláskalová, P and Ilík, V and Tomčala, A and Pavlíčková, Z and Brožová, K and Lukeš, J and Oborník, M and Kolísko, M and Pafčo, B and Jirků, K},
title = {Developmental plasticity enables an intestinal tapeworm to adapt to dietary stress.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-69475-0},
pmid = {41720781},
issn = {2041-1723},
abstract = {Diet is one of the strongest ecological forces shaping the gut environment, yet its impact on intestinal worms (helminths) remains poorly understood. The helminth Hymenolepis diminuta is a suitable model for investigating how lifestyle changes in modern societies may disrupt host-helminth relationships. Here we show that dietary fiber availability shapes the developmental trajectory and life strategies of H. diminuta in a stage-dependent manner. Fiber deprivation at the time of host colonization leads to developmental arrest, manifested by reduced growth, absence of reproduction, and transcriptional changes consistent with suppressed development. This state is accompanied by diet-dependent remodeling of the host small intestinal microbiota and metabolome: whereas fiber-rich diets support fermentative microbial communities and a chemically diverse intestinal environment, the Western diet promotes dysbiotic profiles with reduced fermentation capacity and a more pro-inflammatory immune response. In contrast, adult H. diminuta that reach maturity in hosts maintained on a fiber-rich diet exhibit a reversible, estivation-like suppression of reproduction during short-term fiber deprivation, with full restoration of egg production following dietary recovery. Together, these findings indicate that dietary transitions associated with industrialized lifestyles can redirect helminth developmental programs and host-helminth-microbiome interactions, with implications for helminth persistence and potential therapeutic applications.},
}
RevDate: 2026-02-21
Co-exposure to microplastics and tire particles exacerbates oxidative stress and gut microbiome dysbiosis in zebrafish (Danio rerio).
Environmental research, 296:124069 pii:S0013-9351(26)00397-X [Epub ahead of print].
Microplastics (MPs) and tire particles (TPs) are widespread aquatic pollutants, yet their combined toxic effects, particularly under realistic mixture scenarios, is poorly investigated. In this study, adult zebrafish were chronically exposed for 21 days to environmentally relevant concentrations (1 and 5 mg/L) of mixture of MPs comprising polyethylene terephthalate (PET), polyethylene (PE), and polypropylene (PP) fragments of different sizes (6.5, 13, and 75 μm for each polymer type), as well as PET and PP fibers (300-450 × 18 μm and 300-500 × 20 μm, respectively), TPs alone, and combined MPs and TPs (MPs-TPs). Particle accumulation occurred predominantly in the gut, with secondary deposition in the liver. All exposure groups exhibited oxidative stress responses in gill, gut, and liver tissues, with the most pronounced malondialdehyde (MDA) elevation and antioxidant enzyme disruption observed in the liver under 5 mg/L MPs-TPs exposure, reflecting its central role in detoxification. Gut microbiota analysis revealed significant shifts in community structure and diversity, including reduced Proteobacteria abundance and increased pollutant-tolerant taxa, indicating dysbiosis. Principal Coordinates Analysis (PCoA) confirmed distinct microbial clustering by treatment, indicating that MPs, TPs, and especially MPs-TPs co-exposure caused significant structural reorganization of the gut microbiome. These alterations reflected dysbiosis characterized by disrupted microbial balance, followed by partial recovery indicating microbial resilience. Taken together, these results demonstrate that combined exposure to MPs and TPs results in more severe toxicological effects than exposure to either MPs or TPs alone, highlighting the ecological risks associated with complex contaminant mixtures in aquatic environments.
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@article {pmid41720439,
year = {2026},
author = {Keang, K and Cheng, S and Zhao, X and Wasnik, S and Zhang, H and Cross, JS},
title = {Co-exposure to microplastics and tire particles exacerbates oxidative stress and gut microbiome dysbiosis in zebrafish (Danio rerio).},
journal = {Environmental research},
volume = {296},
number = {},
pages = {124069},
doi = {10.1016/j.envres.2026.124069},
pmid = {41720439},
issn = {1096-0953},
abstract = {Microplastics (MPs) and tire particles (TPs) are widespread aquatic pollutants, yet their combined toxic effects, particularly under realistic mixture scenarios, is poorly investigated. In this study, adult zebrafish were chronically exposed for 21 days to environmentally relevant concentrations (1 and 5 mg/L) of mixture of MPs comprising polyethylene terephthalate (PET), polyethylene (PE), and polypropylene (PP) fragments of different sizes (6.5, 13, and 75 μm for each polymer type), as well as PET and PP fibers (300-450 × 18 μm and 300-500 × 20 μm, respectively), TPs alone, and combined MPs and TPs (MPs-TPs). Particle accumulation occurred predominantly in the gut, with secondary deposition in the liver. All exposure groups exhibited oxidative stress responses in gill, gut, and liver tissues, with the most pronounced malondialdehyde (MDA) elevation and antioxidant enzyme disruption observed in the liver under 5 mg/L MPs-TPs exposure, reflecting its central role in detoxification. Gut microbiota analysis revealed significant shifts in community structure and diversity, including reduced Proteobacteria abundance and increased pollutant-tolerant taxa, indicating dysbiosis. Principal Coordinates Analysis (PCoA) confirmed distinct microbial clustering by treatment, indicating that MPs, TPs, and especially MPs-TPs co-exposure caused significant structural reorganization of the gut microbiome. These alterations reflected dysbiosis characterized by disrupted microbial balance, followed by partial recovery indicating microbial resilience. Taken together, these results demonstrate that combined exposure to MPs and TPs results in more severe toxicological effects than exposure to either MPs or TPs alone, highlighting the ecological risks associated with complex contaminant mixtures in aquatic environments.},
}
RevDate: 2026-02-22
Microbial collaboration in bioelectrochemical systems: Mechanisms and advances towards sustainable biobased products.
Biotechnology advances, 88:108845 pii:S0734-9750(26)00051-0 [Epub ahead of print].
The pursuit of sustainability in the urban world has prompted the development of innovative biobased strategies to mitigate the impact of industrial and human activities on the environment. One such strategy is leveraging microbial collaboration to minimize waste and maximize resource efficiency to unlock the production of biobased products embracing circular bioeconomy in rapidly functioning bio-electrochemical systems (BES). BES is a diversified technology with manifold applications that use microbial interactions at electrode interface to synthesize new products with enhanced substrate utilization, contributing to both environmental sustainability and industrial efficiency. Considering the significance of microbial collaboration, this review article is intended to discuss the types and benefits of microbial interactions in BES, partnerships in a mixed microbiome, between co-cultures, underlying factors, mechanisms, and approaches to enhance the yield and targeted outcome advocating sustainability. This review provides an overview of current research, advances in microbial synergy, and the challenges in optimizing microbial consortia for industrial applications. Probing and harnessing synergies between microbial groups or specific microbes is expected to play a pivotal role in advancing efficient bioelectrochemical platforms and accelerating the transition towards a resilient, biobased economy.
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@article {pmid41720411,
year = {2026},
author = {Modestra, JA and Basha, S},
title = {Microbial collaboration in bioelectrochemical systems: Mechanisms and advances towards sustainable biobased products.},
journal = {Biotechnology advances},
volume = {88},
number = {},
pages = {108845},
doi = {10.1016/j.biotechadv.2026.108845},
pmid = {41720411},
issn = {1873-1899},
abstract = {The pursuit of sustainability in the urban world has prompted the development of innovative biobased strategies to mitigate the impact of industrial and human activities on the environment. One such strategy is leveraging microbial collaboration to minimize waste and maximize resource efficiency to unlock the production of biobased products embracing circular bioeconomy in rapidly functioning bio-electrochemical systems (BES). BES is a diversified technology with manifold applications that use microbial interactions at electrode interface to synthesize new products with enhanced substrate utilization, contributing to both environmental sustainability and industrial efficiency. Considering the significance of microbial collaboration, this review article is intended to discuss the types and benefits of microbial interactions in BES, partnerships in a mixed microbiome, between co-cultures, underlying factors, mechanisms, and approaches to enhance the yield and targeted outcome advocating sustainability. This review provides an overview of current research, advances in microbial synergy, and the challenges in optimizing microbial consortia for industrial applications. Probing and harnessing synergies between microbial groups or specific microbes is expected to play a pivotal role in advancing efficient bioelectrochemical platforms and accelerating the transition towards a resilient, biobased economy.},
}
RevDate: 2026-02-20
Self-sufficient fermentation paradigm for cassava stillage valorization into C6 carboxylic acids: regulatory mechanisms and novel microbe identification.
Bioresource technology pii:S0960-8524(26)00317-2 [Epub ahead of print].
Cassava stillage (CS), a carbohydrate-rich byproduct of bioethanol production, holds significant untapped potential as a renewable resource. Upcycling this problematic wastewater offers great promise for addressing both environmental challenges and the demand for sustainable biochemicals. Here, this study proposed a self-sufficient biotechnological paradigm that directly valorizes CS into medium-chain carboxylic acids (MCCAs, e.g., caproic acid) by integrating lactic acid/butyric acid-type fermentation with microbial chain elongation (CE) by two phase fermentation regulatory. Lactic acid and butyric acid were regulated as dominant products with optimal ratio around 2 from CS degradation, and then chain elongated into caproic acid with optimal pH of 6. pH was found to play a crucial role in controlling product distribution in both phases of fermentation and shaping the microbiome. Meanwhile, chain elongation resilience was also found operational pH-dependent. Metagenomic analysis identified the bacterium Clostridium sp. BUCT163 as a putative lactic acid-driven chain elongating microbe. Whole-genome comparison between Clostridium sp. BUCT163 and Clostridium kluyveri species indicated that the genes encoding lactic acid conversion are not widespread among C. kluyveri populations. The combination of metagenomic-binning and comparative genomic analysis Clostridium sp. BUCT163 was distinguished as the novel potential lactic acid/ethanol-driven chain elongating microbe which successfully provided valuable data sets to link bacterial identities with chain elongating microbes. These findings provide foundation for the resource recovery process from CS in a self-sufficient anaerobic fermentation paradigm and the microbial management of chain elongating systems.
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@article {pmid41720311,
year = {2026},
author = {Liu, C and Ji, M and Wu, W and Shi, Y and Treu, L and Wang, W and Campanaro, S},
title = {Self-sufficient fermentation paradigm for cassava stillage valorization into C6 carboxylic acids: regulatory mechanisms and novel microbe identification.},
journal = {Bioresource technology},
volume = {},
number = {},
pages = {134236},
doi = {10.1016/j.biortech.2026.134236},
pmid = {41720311},
issn = {1873-2976},
abstract = {Cassava stillage (CS), a carbohydrate-rich byproduct of bioethanol production, holds significant untapped potential as a renewable resource. Upcycling this problematic wastewater offers great promise for addressing both environmental challenges and the demand for sustainable biochemicals. Here, this study proposed a self-sufficient biotechnological paradigm that directly valorizes CS into medium-chain carboxylic acids (MCCAs, e.g., caproic acid) by integrating lactic acid/butyric acid-type fermentation with microbial chain elongation (CE) by two phase fermentation regulatory. Lactic acid and butyric acid were regulated as dominant products with optimal ratio around 2 from CS degradation, and then chain elongated into caproic acid with optimal pH of 6. pH was found to play a crucial role in controlling product distribution in both phases of fermentation and shaping the microbiome. Meanwhile, chain elongation resilience was also found operational pH-dependent. Metagenomic analysis identified the bacterium Clostridium sp. BUCT163 as a putative lactic acid-driven chain elongating microbe. Whole-genome comparison between Clostridium sp. BUCT163 and Clostridium kluyveri species indicated that the genes encoding lactic acid conversion are not widespread among C. kluyveri populations. The combination of metagenomic-binning and comparative genomic analysis Clostridium sp. BUCT163 was distinguished as the novel potential lactic acid/ethanol-driven chain elongating microbe which successfully provided valuable data sets to link bacterial identities with chain elongating microbes. These findings provide foundation for the resource recovery process from CS in a self-sufficient anaerobic fermentation paradigm and the microbial management of chain elongating systems.},
}
RevDate: 2026-02-20
Higher-order interactions in auxotroph communities enhance their resilience to resource fluctuations.
Cell systems pii:S2405-4712(25)00324-2 [Epub ahead of print].
Auxotrophs are prevalent in microbial communities, enhancing their diversity and stability-a counterintuitive effect considering their dependence on essential resources from other species. To address the ecological roles of auxotrophs, our study introduced a consumer-resource model (CRM) to capture the complex higher-order interactions within these communities. We also developed an intuitive graphical and algebraic framework, which assesses the feasibility of auxotroph communities and their stability under resource fluctuations and biological invasions. Validated against experimental data from synthetic E. coli auxotroph communities, the model accurately predicted outcomes of community assembly. Our findings highlight the critical role of higher-order interactions and resource dependencies in maintaining the diversity and stability of microbial ecosystems dominated by auxotrophs. A record of this paper's transparent peer review process is included in the supplemental information.
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@article {pmid41720095,
year = {2026},
author = {Wang, T and George, AB and Maslov, S},
title = {Higher-order interactions in auxotroph communities enhance their resilience to resource fluctuations.},
journal = {Cell systems},
volume = {},
number = {},
pages = {101491},
doi = {10.1016/j.cels.2025.101491},
pmid = {41720095},
issn = {2405-4720},
abstract = {Auxotrophs are prevalent in microbial communities, enhancing their diversity and stability-a counterintuitive effect considering their dependence on essential resources from other species. To address the ecological roles of auxotrophs, our study introduced a consumer-resource model (CRM) to capture the complex higher-order interactions within these communities. We also developed an intuitive graphical and algebraic framework, which assesses the feasibility of auxotroph communities and their stability under resource fluctuations and biological invasions. Validated against experimental data from synthetic E. coli auxotroph communities, the model accurately predicted outcomes of community assembly. Our findings highlight the critical role of higher-order interactions and resource dependencies in maintaining the diversity and stability of microbial ecosystems dominated by auxotrophs. A record of this paper's transparent peer review process is included in the supplemental information.},
}
RevDate: 2026-02-20
The immune awakening: Transformative strategies against brain tumors.
Journal of the neurological sciences, 483:125787 pii:S0022-510X(26)00069-9 [Epub ahead of print].
Glioblastoma multiforme remains the primary brain tumor with the highest mortality rate, which is highly resistant to aggressive conventional therapies, owing to its capacity to evade the central nervous system's distinctive immunological barriers. Several mechanisms confer this tumor resistance, such as down-regulation of MHC molecules, secretion of immunosuppressive cytokines, metabolic reprogramming, recruitment of Tregs and myeloid-derived suppressor cells, and heterogeneity reinforced by the blood-tumor barrier and hypoxia. The purpose of this review is to examine the changing field of neuroimmunology, emphasizing the interactions between the immune system and the central nervous system (CNS), immunological resistance mechanisms in GBM, and new developments in immunotherapeutic approaches. A comprehensive literature search was conducted from inception till May 2025 on PubMed, Google Scholar, Cochrane and Clinicaltrials.gov to find relevant studies. The recent findings show that CNS is a highly regulated environment with controlled populations of resident and infiltrating immune cells. GBM exploits these immune barriers through various mechanisms, ultimately creating an immunosuppressive tumor microenvironment. Cancer vaccines, immune checkpoint inhibitors, adoptive cell therapies, and oncolytic viruses, show promise but face challenges like limited BBB penetration, immune suppression, and tumor heterogeneity. The role of the gut microbiome and combinatorial strategies are increasingly recognized as vital in overcoming immunotherapy resistance. Nevertheless, continued research is essential to better understand and thereby overcome resistance and improve clinical outcomes in GBM patients.
Additional Links: PMID-41720042
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@article {pmid41720042,
year = {2026},
author = {Abdullah, A and Malik, T and Shuja, H and Bashir, M and Wamiq, U and Ibrahim, HY and Aamir, MS},
title = {The immune awakening: Transformative strategies against brain tumors.},
journal = {Journal of the neurological sciences},
volume = {483},
number = {},
pages = {125787},
doi = {10.1016/j.jns.2026.125787},
pmid = {41720042},
issn = {1878-5883},
abstract = {Glioblastoma multiforme remains the primary brain tumor with the highest mortality rate, which is highly resistant to aggressive conventional therapies, owing to its capacity to evade the central nervous system's distinctive immunological barriers. Several mechanisms confer this tumor resistance, such as down-regulation of MHC molecules, secretion of immunosuppressive cytokines, metabolic reprogramming, recruitment of Tregs and myeloid-derived suppressor cells, and heterogeneity reinforced by the blood-tumor barrier and hypoxia. The purpose of this review is to examine the changing field of neuroimmunology, emphasizing the interactions between the immune system and the central nervous system (CNS), immunological resistance mechanisms in GBM, and new developments in immunotherapeutic approaches. A comprehensive literature search was conducted from inception till May 2025 on PubMed, Google Scholar, Cochrane and Clinicaltrials.gov to find relevant studies. The recent findings show that CNS is a highly regulated environment with controlled populations of resident and infiltrating immune cells. GBM exploits these immune barriers through various mechanisms, ultimately creating an immunosuppressive tumor microenvironment. Cancer vaccines, immune checkpoint inhibitors, adoptive cell therapies, and oncolytic viruses, show promise but face challenges like limited BBB penetration, immune suppression, and tumor heterogeneity. The role of the gut microbiome and combinatorial strategies are increasingly recognized as vital in overcoming immunotherapy resistance. Nevertheless, continued research is essential to better understand and thereby overcome resistance and improve clinical outcomes in GBM patients.},
}
RevDate: 2026-02-20
Harnessing AMF-plant-microbe systems for heavy metal remediation.
Ecotoxicology and environmental safety, 311:119885 pii:S0147-6513(26)00214-9 [Epub ahead of print].
Soil heavy metal pollution poses a global environmental threat, demanding effective and sustainable remediation strategies. Arbuscular mycorrhizal fungi (AMF) play a multifaceted role in enhancing the remediation of heavy metal (HM)-contaminated soils through extensive hyphal networks that interact with plant roots and soil microbiota. AMF hyphae and their exudates, such as glomalin, directly immobilize metal ions and reduce bioavailability by modifying soil properties (e.g., pH). Furthermore, AMF reshape the rhizosphere microbiome by enriching metal-tolerant bacteria (e.g., Pseudomonas, Bacillus) and fostering synergistic microbial communities via cross-kingdom signaling. Within plants, AMF symbiosis-especially with hyperaccumulators-optimizes root architecture, enhances nutrient and water uptake, stimulates biomass production, and regulates key physiological and molecular responses. These include bolstering antioxidant defenses, maintaining photosynthetic efficiency, and upregulating genes involved in metal transport, compartmentalization, and stress signaling. Field studies confirm the potential of AMF-hyperaccumulator systems in metal extraction and stabilization. However, transitioning from controlled experiments to field applications remains challenging due to the complexity of multipartite interactions and a lack of predictive frameworks. This review critically integrates interdisciplinary insights into a forward-looking perspective, emphasizing the need to shift from empirical approaches to an intelligent, predictive design paradigm. We propose leveraging machine learning to decode interactions among AMF genotypes, plant phenotypes, microbial consortia, and soil properties, enabling the rational design of efficient remediation systems. Ultimately, overcoming barriers to field implementation requires integrating robust science with advanced engineering and supportive policy frameworks.
Additional Links: PMID-41719980
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@article {pmid41719980,
year = {2026},
author = {Xu, Y and Ke, J and Zhang, Y and Chen, X and Wang, Y},
title = {Harnessing AMF-plant-microbe systems for heavy metal remediation.},
journal = {Ecotoxicology and environmental safety},
volume = {311},
number = {},
pages = {119885},
doi = {10.1016/j.ecoenv.2026.119885},
pmid = {41719980},
issn = {1090-2414},
abstract = {Soil heavy metal pollution poses a global environmental threat, demanding effective and sustainable remediation strategies. Arbuscular mycorrhizal fungi (AMF) play a multifaceted role in enhancing the remediation of heavy metal (HM)-contaminated soils through extensive hyphal networks that interact with plant roots and soil microbiota. AMF hyphae and their exudates, such as glomalin, directly immobilize metal ions and reduce bioavailability by modifying soil properties (e.g., pH). Furthermore, AMF reshape the rhizosphere microbiome by enriching metal-tolerant bacteria (e.g., Pseudomonas, Bacillus) and fostering synergistic microbial communities via cross-kingdom signaling. Within plants, AMF symbiosis-especially with hyperaccumulators-optimizes root architecture, enhances nutrient and water uptake, stimulates biomass production, and regulates key physiological and molecular responses. These include bolstering antioxidant defenses, maintaining photosynthetic efficiency, and upregulating genes involved in metal transport, compartmentalization, and stress signaling. Field studies confirm the potential of AMF-hyperaccumulator systems in metal extraction and stabilization. However, transitioning from controlled experiments to field applications remains challenging due to the complexity of multipartite interactions and a lack of predictive frameworks. This review critically integrates interdisciplinary insights into a forward-looking perspective, emphasizing the need to shift from empirical approaches to an intelligent, predictive design paradigm. We propose leveraging machine learning to decode interactions among AMF genotypes, plant phenotypes, microbial consortia, and soil properties, enabling the rational design of efficient remediation systems. Ultimately, overcoming barriers to field implementation requires integrating robust science with advanced engineering and supportive policy frameworks.},
}
RevDate: 2026-02-20
Maternal immunization against group B Streptococcus: Immune correlates, microbiome trade-offs, and global implementation challenges.
Vaccine, 77:128381 pii:S0264-410X(26)00189-1 [Epub ahead of print].
Group B Streptococcus (GBS) remains a leading cause of neonatal sepsis, meningitis, stillbirth, and long-term neurodevelopmental impairment worldwide. Although intrapartum antibiotic prophylaxis (IAP) has substantially reduced early-onset GBS disease in high-income settings and remains an effective and evidence-based intervention, it does not prevent late-onset disease, maternal colonization, or GBS-associated stillbirths, and its implementation is challenging in many low- and middle-income countries (LMICs). Maternal vaccination has therefore emerged as a promising complementary strategy to achieve broader, more equitable prevention of GBS disease. This review critically examines current progress in maternal GBS vaccine development by integrating three interrelated dimensions that will shape future vaccine impact: immune correlates of protection, microbiome-related trade-offs of existing antibiotic-based prevention strategies, and global implementation challenges. We highlight recent advances and remaining uncertainties in defining serological and functional immune correlates required for regulatory decision-making, discuss emerging evidence on microbiome perturbations associated with peripartum antibiotic exposure while emphasizing their currently uncertain clinical significance, and analyze operational and policy considerations relevant to vaccine introduction in LMICs. By moving beyond descriptive summaries of the vaccine development pipeline, this review provides an integrated immunological, biological, and implementation-focused framework to inform vaccine evaluation, regulatory pathways, and policy decisions as maternal GBS vaccines approach licensure and global deployment.
Additional Links: PMID-41719865
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@article {pmid41719865,
year = {2026},
author = {Ikrar, T and Muchsin, W and Sophian, A},
title = {Maternal immunization against group B Streptococcus: Immune correlates, microbiome trade-offs, and global implementation challenges.},
journal = {Vaccine},
volume = {77},
number = {},
pages = {128381},
doi = {10.1016/j.vaccine.2026.128381},
pmid = {41719865},
issn = {1873-2518},
abstract = {Group B Streptococcus (GBS) remains a leading cause of neonatal sepsis, meningitis, stillbirth, and long-term neurodevelopmental impairment worldwide. Although intrapartum antibiotic prophylaxis (IAP) has substantially reduced early-onset GBS disease in high-income settings and remains an effective and evidence-based intervention, it does not prevent late-onset disease, maternal colonization, or GBS-associated stillbirths, and its implementation is challenging in many low- and middle-income countries (LMICs). Maternal vaccination has therefore emerged as a promising complementary strategy to achieve broader, more equitable prevention of GBS disease. This review critically examines current progress in maternal GBS vaccine development by integrating three interrelated dimensions that will shape future vaccine impact: immune correlates of protection, microbiome-related trade-offs of existing antibiotic-based prevention strategies, and global implementation challenges. We highlight recent advances and remaining uncertainties in defining serological and functional immune correlates required for regulatory decision-making, discuss emerging evidence on microbiome perturbations associated with peripartum antibiotic exposure while emphasizing their currently uncertain clinical significance, and analyze operational and policy considerations relevant to vaccine introduction in LMICs. By moving beyond descriptive summaries of the vaccine development pipeline, this review provides an integrated immunological, biological, and implementation-focused framework to inform vaccine evaluation, regulatory pathways, and policy decisions as maternal GBS vaccines approach licensure and global deployment.},
}
RevDate: 2026-02-20
Insights into the mechanism of treatment of ulcerative colitis with pre- and post-processed dried ginger through perspective of metabolomics and intestinal microbiomics research.
Journal of pharmaceutical and biomedical analysis, 274:117420 pii:S0731-7085(26)00088-9 [Epub ahead of print].
Numerous experiments and clinical practices have demonstrated the distinct therapeutic effect of dried ginger (DG) and processed ginger (PG) in the treatment of ulcerative colitis (UC), while, the differences in efficacy and mechanisms are not yet fully understood. By integrating metabolomics and gut microbiome analyses, combined with liquid chromatography-mass spectrometry technology for serum metabolism detection, 16S rRNA gene microbiota sequencing and Spearman correlation analysis, the pharmacological effects and mechanisms of action of the two were explored. Pharmacodynamic results demonstrated that both DG and PG have significant therapeutic effects on UC mice, and PG has a better effect in shortening the coagulation time and promoting hemostasis. Metabolomics analysis revealed that DG has 94 differential metabolites, mainly affecting the metabolism of arachidonic acid, whereas PG has 88 differential metabolites, focusing on pathways such as steroid biosynthesis. Intestinal microbiomics analysis indicates that DG and PG can regulate the richness and diversity of the microbiota. DG significantly regulated 3 bacterial families and 8 bacterial genera, while PG regulated 4 families and 11 genera. Spearman correlation analysis further confirmed that PG reshapes the "gut microbiota-host metabolism" interaction network. This study combined multi-omics techniques to analyze the microbiota-metabolism regulatory characteristics of DG and PG in the treatment of UC, and clarified how the component changes caused by ginger processing led to the differentiation of the two in terms of therapeutic focus and the microbiota-metabolism regulatory network. These findings provide scientific evidence supporting the precise application of ginger-derived medicinal materials in the treatment of UC.
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@article {pmid41719786,
year = {2026},
author = {Han, S and Yang, X and Du, J and Hou, Z and Wei, W and Huo, J and Cui, X and Yao, T and Xu, H},
title = {Insights into the mechanism of treatment of ulcerative colitis with pre- and post-processed dried ginger through perspective of metabolomics and intestinal microbiomics research.},
journal = {Journal of pharmaceutical and biomedical analysis},
volume = {274},
number = {},
pages = {117420},
doi = {10.1016/j.jpba.2026.117420},
pmid = {41719786},
issn = {1873-264X},
abstract = {Numerous experiments and clinical practices have demonstrated the distinct therapeutic effect of dried ginger (DG) and processed ginger (PG) in the treatment of ulcerative colitis (UC), while, the differences in efficacy and mechanisms are not yet fully understood. By integrating metabolomics and gut microbiome analyses, combined with liquid chromatography-mass spectrometry technology for serum metabolism detection, 16S rRNA gene microbiota sequencing and Spearman correlation analysis, the pharmacological effects and mechanisms of action of the two were explored. Pharmacodynamic results demonstrated that both DG and PG have significant therapeutic effects on UC mice, and PG has a better effect in shortening the coagulation time and promoting hemostasis. Metabolomics analysis revealed that DG has 94 differential metabolites, mainly affecting the metabolism of arachidonic acid, whereas PG has 88 differential metabolites, focusing on pathways such as steroid biosynthesis. Intestinal microbiomics analysis indicates that DG and PG can regulate the richness and diversity of the microbiota. DG significantly regulated 3 bacterial families and 8 bacterial genera, while PG regulated 4 families and 11 genera. Spearman correlation analysis further confirmed that PG reshapes the "gut microbiota-host metabolism" interaction network. This study combined multi-omics techniques to analyze the microbiota-metabolism regulatory characteristics of DG and PG in the treatment of UC, and clarified how the component changes caused by ginger processing led to the differentiation of the two in terms of therapeutic focus and the microbiota-metabolism regulatory network. These findings provide scientific evidence supporting the precise application of ginger-derived medicinal materials in the treatment of UC.},
}
RevDate: 2026-02-20
Adenosine signaling driven by the gut microbiota underlies chronic alcohol-induced anesthetic resistance.
Cell reports, 45(3):117015 pii:S2211-1247(26)00093-8 [Epub ahead of print].
Chronic alcohol consumption increases anesthetic tolerance, yet the underlying in vivo mechanisms remain unclear. Here, we demonstrate that long-term alcohol exposure reduces anesthetic efficacy in both humans and mice, prolonging induction and shortening maintenance. Fecal microbiota transplantation from alcohol-exposed donors recapitulated this phenotype in naive mice, indicating a causal role of gut microbiome alterations. Metagenomic and metabolomic analyses identified elevated adenosine as a key microbiota-derived metabolite. Adenosine supplementation decreased anesthetic sensitivity, likely via downregulation of gamma-aminobutyric acid (GABA) receptors. Our findings reveal a gut microbiota-adenosine pathway mediating alcohol-induced anesthetic resistance.
Additional Links: PMID-41719127
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@article {pmid41719127,
year = {2026},
author = {Wang, S and Su, LY and Lan, D and Pan, H and Xiong, M and Yao, M and Deng, Y and Fan, Z and Cao, Y and Zhou, H},
title = {Adenosine signaling driven by the gut microbiota underlies chronic alcohol-induced anesthetic resistance.},
journal = {Cell reports},
volume = {45},
number = {3},
pages = {117015},
doi = {10.1016/j.celrep.2026.117015},
pmid = {41719127},
issn = {2211-1247},
abstract = {Chronic alcohol consumption increases anesthetic tolerance, yet the underlying in vivo mechanisms remain unclear. Here, we demonstrate that long-term alcohol exposure reduces anesthetic efficacy in both humans and mice, prolonging induction and shortening maintenance. Fecal microbiota transplantation from alcohol-exposed donors recapitulated this phenotype in naive mice, indicating a causal role of gut microbiome alterations. Metagenomic and metabolomic analyses identified elevated adenosine as a key microbiota-derived metabolite. Adenosine supplementation decreased anesthetic sensitivity, likely via downregulation of gamma-aminobutyric acid (GABA) receptors. Our findings reveal a gut microbiota-adenosine pathway mediating alcohol-induced anesthetic resistance.},
}
RevDate: 2026-02-20
Forensic microbiome research: the critical gap between proof of concept and proof of utility.
Additional Links: PMID-41718999
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@article {pmid41718999,
year = {2026},
author = {Wang, Q},
title = {Forensic microbiome research: the critical gap between proof of concept and proof of utility.},
journal = {Forensic science, medicine, and pathology},
volume = {},
number = {},
pages = {},
pmid = {41718999},
issn = {1556-2891},
}
RevDate: 2026-02-20
Cadmium-Induced Microbiome Dysbiosis Promotes Potato Late Blight in Karst Soils.
Bulletin of environmental contamination and toxicology, 116(3):.
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@article {pmid41718760,
year = {2026},
author = {Li, C and Liu, H and Wang, X and Zhang, R and Zhang, H and Gu, Z},
title = {Cadmium-Induced Microbiome Dysbiosis Promotes Potato Late Blight in Karst Soils.},
journal = {Bulletin of environmental contamination and toxicology},
volume = {116},
number = {3},
pages = {},
pmid = {41718760},
issn = {1432-0800},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Extracellular vesicles and their RNA cargo facilitate bidirectional cross-kingdom communication between human and bacterial cells.
Gut microbes, 18(1):2630482.
While extracellular vesicles (EVs) are established mediators of intra-species signaling, their contribution to cross-kingdom communication remains incompletely understood. Here, we investigate the EV-mediated interactions between human colon epithelial cells and both Gram-positive and Gram-negative gut bacteria. We show that bacterial EVs (BEVs) derived from Lacticaseibacillus casei, Enterococcus faecalis, and Proteus mirabilis induce distinct transcriptomic changes in Caco-2 cells depending on the bacterial species, with up to ~6,000 differentially expressed genes, including CCL20, CXCL8, or CXCL10. Transfection of BEV-derived RNA independently induces a subset of similar effects, indicating that the EV-mediated communication is partially driven by the RNA cargo. Conversely, we demonstrate that bacteria interact with Caco-2-derived EVs and miR-192-5p, which is highly abundant (~36.4-fold higher) in EVs isolated from conditioned medium compared with EVs from unconditioned medium, with modest effects on bacterial growth. Furthermore, we show that lipid-based packaging of miR-192-5p modulates its association with the bacteria. Our findings support a conceptual model in which EVs and their RNA cargo contribute to species-dependent host-microbe interactions. This study introduces a framework for understanding EVs as cross-kingdom regulators and underscores the importance of tailored, context-specific analyses for understanding the scope of EV-mediated interactions in microbiome-host homeostasis and disease.
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@article {pmid41718551,
year = {2026},
author = {Gröger, L and Rishik, S and Ludwig, N and Beganovic, A and Koch, M and Rheinheimer, S and Hart, M and König, P and Trampert, T and Paul, P and Boese, A and Lehr, CM and Becker, SL and Fuhrmann, G and Keller, A and Meese, E},
title = {Extracellular vesicles and their RNA cargo facilitate bidirectional cross-kingdom communication between human and bacterial cells.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2630482},
doi = {10.1080/19490976.2026.2630482},
pmid = {41718551},
issn = {1949-0984},
mesh = {Humans ; *Extracellular Vesicles/metabolism/genetics ; MicroRNAs/metabolism/genetics ; Caco-2 Cells ; *RNA, Bacterial/metabolism/genetics ; *Epithelial Cells/microbiology/metabolism ; *Gastrointestinal Microbiome ; },
abstract = {While extracellular vesicles (EVs) are established mediators of intra-species signaling, their contribution to cross-kingdom communication remains incompletely understood. Here, we investigate the EV-mediated interactions between human colon epithelial cells and both Gram-positive and Gram-negative gut bacteria. We show that bacterial EVs (BEVs) derived from Lacticaseibacillus casei, Enterococcus faecalis, and Proteus mirabilis induce distinct transcriptomic changes in Caco-2 cells depending on the bacterial species, with up to ~6,000 differentially expressed genes, including CCL20, CXCL8, or CXCL10. Transfection of BEV-derived RNA independently induces a subset of similar effects, indicating that the EV-mediated communication is partially driven by the RNA cargo. Conversely, we demonstrate that bacteria interact with Caco-2-derived EVs and miR-192-5p, which is highly abundant (~36.4-fold higher) in EVs isolated from conditioned medium compared with EVs from unconditioned medium, with modest effects on bacterial growth. Furthermore, we show that lipid-based packaging of miR-192-5p modulates its association with the bacteria. Our findings support a conceptual model in which EVs and their RNA cargo contribute to species-dependent host-microbe interactions. This study introduces a framework for understanding EVs as cross-kingdom regulators and underscores the importance of tailored, context-specific analyses for understanding the scope of EV-mediated interactions in microbiome-host homeostasis and disease.},
}
MeSH Terms:
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Humans
*Extracellular Vesicles/metabolism/genetics
MicroRNAs/metabolism/genetics
Caco-2 Cells
*RNA, Bacterial/metabolism/genetics
*Epithelial Cells/microbiology/metabolism
*Gastrointestinal Microbiome
RevDate: 2026-02-22
CmpDate: 2026-02-20
Microbiome-Metabolome Crosstalk as a Driver of COVID-19 Severity.
Medical sciences (Basel, Switzerland), 14(1):.
Background: COVID-19, caused by SARS-CoV-2, exhibits highly variable severity, from mild symptoms to respiratory failure and multiorgan dysfunction. Traditional risk factors incompletely explain this heterogeneity, highlighting the potential role of gut microbiota and host metabolomics in modulating immune responses. Methods: Thus, this study investigates how gut microbiota variations are associated with plasma metabolite profiles in COVID-19, exploring relationships between microbial and metabolic signatures and disease severity and potential therapeutic targets. In a prospective cohort of 55 patients, stool and plasma samples were analyzed using 16S rRNA sequencing and untargeted LC-HRMS metabolomics. Results: Severe COVID-19 was associated with reduced microbial diversity and enrichment of pro-inflammatory taxa, including Prevotella, Alistipes, Dialister, and Lachnoclostridium, whereas mild cases showed higher abundance of protective commensals such as Bacteroides, Faecalibacterium, and Blautia. Metabolomic profiling revealed alterations in bile acids, unsaturated fatty acids, tryptophan, and inositol phosphate pathways. Notably, linoleate levels were elevated in severe cases, showing correlations with pro-inflammatory microbes, while acylcarnitines and inositol derivatives were enriched in mild disease. Predictive functional analysis suggested that severe-associated microbes showed enhanced amino acid catabolism, oxidative glucose metabolism, and xenobiotic degradation, which may be linked to host inflammation. Conclusions: These findings highlight associations between gut microbiota composition, microbial metabolism, and circulating metabolites in COVID-19 severity. Identified microbial and metabolomic signatures may represent potential candidates to be considered biomarkers and therapeutic targets to modulate disease progression.
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@article {pmid41718144,
year = {2026},
author = {Diez-Echave, P and Rodríguez-Sojo, MJ and Martin-Castaño, B and Hidalgo-García, L and Ruiz-Malagon, AJ and Molina-Tijeras, JA and Romero, AR and Martínez-Zaldívar, M and Mota, E and Cobo, F and Alvarez-Estevez, M and García, F and Morales-García, C and Merlos, S and García-Flores, P and Colmenero-Ruiz, M and Nuñez, M and Ruiz-Sancho, A and Rodríguez-Cabezas, ME and Gallego, ÁC and Fernandez-Varón, E and Pérez Del Palacio, J and Martin, J and García-García, J and Morón, R and Rodríguez-Nogales, A and Gálvez, J},
title = {Microbiome-Metabolome Crosstalk as a Driver of COVID-19 Severity.},
journal = {Medical sciences (Basel, Switzerland)},
volume = {14},
number = {1},
pages = {},
pmid = {41718144},
issn = {2076-3271},
support = {CV20-99908//Andalusian Health Service/ ; },
mesh = {Humans ; *COVID-19/microbiology/metabolism ; *Gastrointestinal Microbiome ; Male ; Middle Aged ; Female ; Severity of Illness Index ; SARS-CoV-2 ; *Metabolome ; Prospective Studies ; Aged ; Metabolomics/methods ; Adult ; Feces/microbiology ; RNA, Ribosomal, 16S/genetics ; },
abstract = {Background: COVID-19, caused by SARS-CoV-2, exhibits highly variable severity, from mild symptoms to respiratory failure and multiorgan dysfunction. Traditional risk factors incompletely explain this heterogeneity, highlighting the potential role of gut microbiota and host metabolomics in modulating immune responses. Methods: Thus, this study investigates how gut microbiota variations are associated with plasma metabolite profiles in COVID-19, exploring relationships between microbial and metabolic signatures and disease severity and potential therapeutic targets. In a prospective cohort of 55 patients, stool and plasma samples were analyzed using 16S rRNA sequencing and untargeted LC-HRMS metabolomics. Results: Severe COVID-19 was associated with reduced microbial diversity and enrichment of pro-inflammatory taxa, including Prevotella, Alistipes, Dialister, and Lachnoclostridium, whereas mild cases showed higher abundance of protective commensals such as Bacteroides, Faecalibacterium, and Blautia. Metabolomic profiling revealed alterations in bile acids, unsaturated fatty acids, tryptophan, and inositol phosphate pathways. Notably, linoleate levels were elevated in severe cases, showing correlations with pro-inflammatory microbes, while acylcarnitines and inositol derivatives were enriched in mild disease. Predictive functional analysis suggested that severe-associated microbes showed enhanced amino acid catabolism, oxidative glucose metabolism, and xenobiotic degradation, which may be linked to host inflammation. Conclusions: These findings highlight associations between gut microbiota composition, microbial metabolism, and circulating metabolites in COVID-19 severity. Identified microbial and metabolomic signatures may represent potential candidates to be considered biomarkers and therapeutic targets to modulate disease progression.},
}
MeSH Terms:
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Humans
*COVID-19/microbiology/metabolism
*Gastrointestinal Microbiome
Male
Middle Aged
Female
Severity of Illness Index
SARS-CoV-2
*Metabolome
Prospective Studies
Aged
Metabolomics/methods
Adult
Feces/microbiology
RNA, Ribosomal, 16S/genetics
RevDate: 2026-02-20
Environmental Stress Induces Altered Composition of Streptococcus mutans Membrane Vesicles: pH-Driven Changes in Membrane Vesicle Production and Composition.
Molecular oral microbiology [Epub ahead of print].
Bacteria produce membrane vesicles (MVs) in response to environmental stress and genetic changes. Previous studies have shown that MVs can trigger inflammatory responses and may serve as important mediators of host-microbe interactions. Given the dynamic nature of the oral microbiome, bacteria such as Streptococcus mutans are frequently exposed to environmental fluctuations that could alter MV production. The objective of this study was to investigate whether inducing stress conditions would affect MV production and morphology in S. mutans, a prominent oral pathogen. Cultures were subjected to different pH conditions to mimic environmentally relevant stress. MVs were isolated and purified in order to characterize and assess changes in yield, size, and cargo. Our findings show that acidic stress significantly increased MV production while reducing average MV size. We also observed significant differences in MV content when compared to control conditions. These changes may reflect bacterial adaptation strategies and could influence how MVs interact with host immune systems. Overall, this study highlights the potential for environmental stress to reshape MV-mediated communication in the oral microbiome and provides a foundation for exploring how such changes may contribute to inflammation and oral disease.
Additional Links: PMID-41718018
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PubMed:
Citation:
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@article {pmid41718018,
year = {2026},
author = {Boone, TC and Shankar, SK and Weller, ML},
title = {Environmental Stress Induces Altered Composition of Streptococcus mutans Membrane Vesicles: pH-Driven Changes in Membrane Vesicle Production and Composition.},
journal = {Molecular oral microbiology},
volume = {},
number = {},
pages = {e70022},
doi = {10.1111/omi.70022},
pmid = {41718018},
issn = {2041-1014},
abstract = {Bacteria produce membrane vesicles (MVs) in response to environmental stress and genetic changes. Previous studies have shown that MVs can trigger inflammatory responses and may serve as important mediators of host-microbe interactions. Given the dynamic nature of the oral microbiome, bacteria such as Streptococcus mutans are frequently exposed to environmental fluctuations that could alter MV production. The objective of this study was to investigate whether inducing stress conditions would affect MV production and morphology in S. mutans, a prominent oral pathogen. Cultures were subjected to different pH conditions to mimic environmentally relevant stress. MVs were isolated and purified in order to characterize and assess changes in yield, size, and cargo. Our findings show that acidic stress significantly increased MV production while reducing average MV size. We also observed significant differences in MV content when compared to control conditions. These changes may reflect bacterial adaptation strategies and could influence how MVs interact with host immune systems. Overall, this study highlights the potential for environmental stress to reshape MV-mediated communication in the oral microbiome and provides a foundation for exploring how such changes may contribute to inflammation and oral disease.},
}
RevDate: 2026-02-20
Altered Nasal Microbiota in Sinonasal Tumors: A Comparative Analysis of Malignant and Benign Sinonasal Tumors.
International forum of allergy & rhinology [Epub ahead of print].
BACKGROUND: Although shifts in nasal microbiota have been well-documented in inflammatory upper airway conditions, microbiota tumor-associated alterations remain uncharacterized. This study is the first to compare sinonasal microbiota profiles of patients with malignant tumors (MT), benign tumors (BT), and controls, offering insights into tumor-associated microbiomes.
METHODS: This prospective, cross-sectional, observational study assessed intraoperative sinus swabs from 70 adult research participants (MT = 23, BT = 15, control = 32). Sinonasal microbial communities were characterized using 16S rRNA gene amplicon sequencing to determine if microbial community structures differed between groups.
RESULTS: Tumor-associated sinonasal microbiota profiles showed clear dysbiosis, with reduced relative abundance of beneficial microbes and increased putative pathogenic taxa. Both MT and BT had significantly lower microbial diversity and distinct compositions compared to controls. MT samples had significantly higher relative abundance of Firmicutes and reduced relative abundance of Actinobacteria. These phylum-level alterations were accompanied by elevated proinflammatory microbial taxa, paired with reduced relative abundance of keystone, beneficial taxa consistent with healthy nasal microbiomes. Microbial communities in BT and MT samples were similar, but Alcaligenes was more abundant, and Corynebacterium was less abundant in MT than in BT.
CONCLUSION: This study observed that sinonasal microbial communities in MT exhibited marked dysbiosis with a reduction in the relative abundance of putative sinonasal commensal taxa compared to controls. These alterations were present to a lesser extent in BT. Future investigations should aim to determine whether these microbial shifts contribute to tumor development or represent secondary effects, with an aim to quantify their impact on outcomes and guide therapeutic strategies.
Additional Links: PMID-41717863
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PubMed:
Citation:
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@article {pmid41717863,
year = {2026},
author = {Patel, EA and Engen, PA and Souza, GD and Khalife, S and Moore, D and Kret, L and Escobedo, P and Green, SJ and Naqib, A and Filip, P and Papagiannopoulos, P and Tajudeen, BA and Mahdavinia, M and Batra, PS},
title = {Altered Nasal Microbiota in Sinonasal Tumors: A Comparative Analysis of Malignant and Benign Sinonasal Tumors.},
journal = {International forum of allergy & rhinology},
volume = {},
number = {},
pages = {},
doi = {10.1002/alr.70123},
pmid = {41717863},
issn = {2042-6984},
support = {//Miller Family Foundation/ ; },
abstract = {BACKGROUND: Although shifts in nasal microbiota have been well-documented in inflammatory upper airway conditions, microbiota tumor-associated alterations remain uncharacterized. This study is the first to compare sinonasal microbiota profiles of patients with malignant tumors (MT), benign tumors (BT), and controls, offering insights into tumor-associated microbiomes.
METHODS: This prospective, cross-sectional, observational study assessed intraoperative sinus swabs from 70 adult research participants (MT = 23, BT = 15, control = 32). Sinonasal microbial communities were characterized using 16S rRNA gene amplicon sequencing to determine if microbial community structures differed between groups.
RESULTS: Tumor-associated sinonasal microbiota profiles showed clear dysbiosis, with reduced relative abundance of beneficial microbes and increased putative pathogenic taxa. Both MT and BT had significantly lower microbial diversity and distinct compositions compared to controls. MT samples had significantly higher relative abundance of Firmicutes and reduced relative abundance of Actinobacteria. These phylum-level alterations were accompanied by elevated proinflammatory microbial taxa, paired with reduced relative abundance of keystone, beneficial taxa consistent with healthy nasal microbiomes. Microbial communities in BT and MT samples were similar, but Alcaligenes was more abundant, and Corynebacterium was less abundant in MT than in BT.
CONCLUSION: This study observed that sinonasal microbial communities in MT exhibited marked dysbiosis with a reduction in the relative abundance of putative sinonasal commensal taxa compared to controls. These alterations were present to a lesser extent in BT. Future investigations should aim to determine whether these microbial shifts contribute to tumor development or represent secondary effects, with an aim to quantify their impact on outcomes and guide therapeutic strategies.},
}
RevDate: 2026-02-20
Multiple Roles and Therapeutic Targets of Tuft Cells in Inflammatory Bowel Disease.
Journal of gastroenterology and hepatology [Epub ahead of print].
Tuft cells are rare epithelial chemosensory cells located in diverse organs, including the gut tract, and are characterized by large apical protrusions. Known as gut sentinels, tuft cells release widespread immunological effector molecules in response to gut luminal pathogens. Specifically, tuft cells are major regulators in initiating immune responses against certain nematodes and parasites. Another tuft cell property is the maintenance of gut hemostasis and modulation of the gut microbiome, which reduces intestinal inflammation. On the other hand, the pathophysiology of inflammatory bowel disease (IBD) is strongly linked to dysregulated immune responses, imbalances in the gut microbiome, and disruption of the mucosal barrier integrity. Hence, this review discusses tuft cell-mediated immune system response and its activation through luminal pathogens. It also addresses how the succinate-tuft cell axis plays a role in gut microbiome modulation. Finally, therapeutic options of tuft cell molecular effectors and their signaling pathways in IBD treatment are highlighted.
Additional Links: PMID-41717814
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PubMed:
Citation:
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@article {pmid41717814,
year = {2026},
author = {Masir, MN},
title = {Multiple Roles and Therapeutic Targets of Tuft Cells in Inflammatory Bowel Disease.},
journal = {Journal of gastroenterology and hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jgh.70298},
pmid = {41717814},
issn = {1440-1746},
abstract = {Tuft cells are rare epithelial chemosensory cells located in diverse organs, including the gut tract, and are characterized by large apical protrusions. Known as gut sentinels, tuft cells release widespread immunological effector molecules in response to gut luminal pathogens. Specifically, tuft cells are major regulators in initiating immune responses against certain nematodes and parasites. Another tuft cell property is the maintenance of gut hemostasis and modulation of the gut microbiome, which reduces intestinal inflammation. On the other hand, the pathophysiology of inflammatory bowel disease (IBD) is strongly linked to dysregulated immune responses, imbalances in the gut microbiome, and disruption of the mucosal barrier integrity. Hence, this review discusses tuft cell-mediated immune system response and its activation through luminal pathogens. It also addresses how the succinate-tuft cell axis plays a role in gut microbiome modulation. Finally, therapeutic options of tuft cell molecular effectors and their signaling pathways in IBD treatment are highlighted.},
}
RevDate: 2026-02-20
Microbial synthesis structures organic compound composition in anaerobic digestion.
The ISME journal pii:8492921 [Epub ahead of print].
Anaerobic digestion (AD) is a cornerstone technology for sustainable waste treatment and renewable energy recovery, yet its complex microbe-metabolite interactions remain poorly understood. Here, we combined high-resolution molecular profiling and microbial community sequencing in a three-month study across seven full-scale digesters to resolve dissolved organic matter (DOM) and microbiome dynamics. A total of 28,925 DOM molecules, including a conserved core of 1,154 metabolites, were identified. By disentangling metabolic pathways, we observed complex transformation patterns that extend beyond simple substrate breakdown. Molecules within a mass window (183.57-390.81 m/z) exhibited high persistence, strong microbial associations, and distinct transformation trajectories. Within this mass window, microbial community composition and feedstock input, together explained ~30.1%-43.4% of the observed spatiotemporal variation. In each digester, 1,260-2,108 molecules were closely associated with microbial metabolism, forming 7.77-24.52 microbe-metabolite associations on average. The accumulation and turnover of these microbial metabolites were strongly linked to methane production and system performance, highlighting microbial processing of DOM as a significant factor shaping microbe-metabolite interactions. This perspective emphasizes the importance of microbe-metabolite interplay in AD, providing a conceptual framework for predictive monitoring and optimization of engineered biotechnologies.
Additional Links: PMID-41717792
Publisher:
PubMed:
Citation:
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@article {pmid41717792,
year = {2026},
author = {Yang, X and Zhao, B and Feng, K and Wang, J and Liu, M and Peng, X and He, Q and Lu, Y and Waseem, H and Wang, S and Winkler, MH and Salles, JF and Deng, Y},
title = {Microbial synthesis structures organic compound composition in anaerobic digestion.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag036},
pmid = {41717792},
issn = {1751-7370},
abstract = {Anaerobic digestion (AD) is a cornerstone technology for sustainable waste treatment and renewable energy recovery, yet its complex microbe-metabolite interactions remain poorly understood. Here, we combined high-resolution molecular profiling and microbial community sequencing in a three-month study across seven full-scale digesters to resolve dissolved organic matter (DOM) and microbiome dynamics. A total of 28,925 DOM molecules, including a conserved core of 1,154 metabolites, were identified. By disentangling metabolic pathways, we observed complex transformation patterns that extend beyond simple substrate breakdown. Molecules within a mass window (183.57-390.81 m/z) exhibited high persistence, strong microbial associations, and distinct transformation trajectories. Within this mass window, microbial community composition and feedstock input, together explained ~30.1%-43.4% of the observed spatiotemporal variation. In each digester, 1,260-2,108 molecules were closely associated with microbial metabolism, forming 7.77-24.52 microbe-metabolite associations on average. The accumulation and turnover of these microbial metabolites were strongly linked to methane production and system performance, highlighting microbial processing of DOM as a significant factor shaping microbe-metabolite interactions. This perspective emphasizes the importance of microbe-metabolite interplay in AD, providing a conceptual framework for predictive monitoring and optimization of engineered biotechnologies.},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Pulpitis as a microbial disease: single-cell insights into host responses and diagnostic biomarkers for vital pulp therapy.
Journal of oral microbiology, 18(1):2622207.
BACKGROUND: Pulpitis is a common dental disease driven by complex microbial infections, yet its microbial origins, diversity, and pathogenic mechanisms remain incompletely understood. A major clinical challenge is the absence of objective biological criteria to assess the severity and reversibility of pulpal inflammation, which is essential for decision-making in vital pulp therapy (VPT).
OBJECTIVE: This review aims to synthesize current evidence on the microbial landscape of pulpitis and to explore microbial- and host-derived biomarkers that may enable objective assessment of inflammation severity and support precision VPT.
DESIGN: We comprehensively reviewed microorganisms implicated in pulpitis and their distinct virulence mechanisms underlying inflammatory responses and tissue damage. Particular emphasis was placed on host responses of dental pulp stem cells (DPSCs) to different microbial infections. Biomarker candidates reported across multiple studies were summarized, and single-cell transcriptomic evidence was integrated to validate microbe-specific DPSC responses.
RESULTS: Distinct microorganisms associated with pulpitis exhibit heterogeneous virulence strategies, inducing diverse inflammatory and degenerative processes within the dental pulp. DPSCs display infection-specific transcriptional responses, revealing molecular signatures linked to inflammation severity and tissue repair potential. Emerging biomarkers derived from both microbial factors and host responses show consistency across studies, with single-cell analyses providing high-resolution validation of these microbe-specific patterns.
CONCLUSIONS: Microbial- and host-derived biomarkers hold significant translational potential for stratifying pulpitis severity, informing VPT decision-making, and predicting treatment prognosis. Integrating microbial characterization with host response profiling may advance objective diagnosis and personalized management of pulpitis.
Additional Links: PMID-41717505
PubMed:
Citation:
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@article {pmid41717505,
year = {2026},
author = {Xu, T and Yang, D and Zhang, L and Li, M and Li, X and Duan, C and Cheung, Y and Zhang, W and Zhang, Z and Yue, L and Zou, X and Chen, F},
title = {Pulpitis as a microbial disease: single-cell insights into host responses and diagnostic biomarkers for vital pulp therapy.},
journal = {Journal of oral microbiology},
volume = {18},
number = {1},
pages = {2622207},
pmid = {41717505},
issn = {2000-2297},
abstract = {BACKGROUND: Pulpitis is a common dental disease driven by complex microbial infections, yet its microbial origins, diversity, and pathogenic mechanisms remain incompletely understood. A major clinical challenge is the absence of objective biological criteria to assess the severity and reversibility of pulpal inflammation, which is essential for decision-making in vital pulp therapy (VPT).
OBJECTIVE: This review aims to synthesize current evidence on the microbial landscape of pulpitis and to explore microbial- and host-derived biomarkers that may enable objective assessment of inflammation severity and support precision VPT.
DESIGN: We comprehensively reviewed microorganisms implicated in pulpitis and their distinct virulence mechanisms underlying inflammatory responses and tissue damage. Particular emphasis was placed on host responses of dental pulp stem cells (DPSCs) to different microbial infections. Biomarker candidates reported across multiple studies were summarized, and single-cell transcriptomic evidence was integrated to validate microbe-specific DPSC responses.
RESULTS: Distinct microorganisms associated with pulpitis exhibit heterogeneous virulence strategies, inducing diverse inflammatory and degenerative processes within the dental pulp. DPSCs display infection-specific transcriptional responses, revealing molecular signatures linked to inflammation severity and tissue repair potential. Emerging biomarkers derived from both microbial factors and host responses show consistency across studies, with single-cell analyses providing high-resolution validation of these microbe-specific patterns.
CONCLUSIONS: Microbial- and host-derived biomarkers hold significant translational potential for stratifying pulpitis severity, informing VPT decision-making, and predicting treatment prognosis. Integrating microbial characterization with host response profiling may advance objective diagnosis and personalized management of pulpitis.},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Ramulus mori (Sangzhi) alkaloids improve intestinal oxidative damage and inflammation in DHEA-induced polycystic ovary syndrome rats via gut microbiota and metabolite modulation.
Frontiers in pharmacology, 16:1701694.
INTRODUCTION: Intestinal dysbiosis, characterized by reduced diversity and enrichment of pro-inflammatory taxa, is implicated in the pathogenesis of polycystic ovary syndrome (PCOS). Ramulus mori (Sangzhi) alkaloids (SZ-A), approved in China for type 2 diabetes with broad metabolic effects, remain untested as a microbiota-targeted intervention for PCOS.
METHODS: In a dehydroepiandrosterone (DHEA)-induced rat model of PCOS, we evaluated the therapeutic efficacy of SZ-A and its underlying microbiota-metabolite interactions through integrated assessments of reproductive and endocrine-metabolic function, oxidative stress, inflammatory cytokines, and gut microbiota and serum metabolite profiles.
RESULTS: Relative to SD rats, PCOS rats showed approximately 10-fold higher cystic follicle burden and a one-third reduction in corpora lutea, with serum testosterone rising from 0.12 ± 0.08 to 0.27 ± 0.08 ng/mL, total bile acids falling from 34.22 ± 5.52 to 20.63 ± 4.94 μM, and HOMA-IR significantly increased (all p < 0.05). SZ-A treatment reduced cystic follicles, restored estrous cyclicity and luteal formation, and shifted testosterone, total bile acids, and HOMA-IR toward SD levels. At the molecular level, SZ-A appears to act by remodeling gut microbiota composition and serum metabolite profiles. SZ-A significantly shifted microbial β-diversity in PCOS rats while retaining a community dominated by Bacteroidetes and Firmicutes with Lactobacillus and Treponema_2 as key genera. Untargeted metabolomics identified 13 PCOS-associated serum metabolites that were significantly reduced after SZ-A treatment (p < 0.05), highlighting fenoldopam as a putative mediator of its beneficial effects on ovarian function and metabolic homeostasis. With respect to oxidative injury, serum malondialdehyde (MDA) levels in PCOS rats were approximately twice those of the SD group, while total antioxidant capacity (T-AOC) and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were significantly reduced (p < 0.05); treatment with SZ-A markedly attenuated these alterations (p < 0.05). Besides, it suppressed systemic inflammation by reducing interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) levels in serum and relevant tissues (p < 0.05).
DISCUSSION: Collectively, these findings indicate that SZ-A alleviates PCOS by attenuating intestinal oxidative stress and normalizing gut microbiota-metabolite interactions, and highlight fenoldopam as a potential effector, supporting SZ-A as a promising therapeutic candidate for PCOS.
Additional Links: PMID-41717482
PubMed:
Citation:
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@article {pmid41717482,
year = {2025},
author = {Wang, Y and Jiang, X and Wu, S and Wang, Q and Zuo, D and Huang, B and Jian, L and Yang, Y and Cai, Y and Wen, X and Yao, L and Geng, S},
title = {Ramulus mori (Sangzhi) alkaloids improve intestinal oxidative damage and inflammation in DHEA-induced polycystic ovary syndrome rats via gut microbiota and metabolite modulation.},
journal = {Frontiers in pharmacology},
volume = {16},
number = {},
pages = {1701694},
pmid = {41717482},
issn = {1663-9812},
abstract = {INTRODUCTION: Intestinal dysbiosis, characterized by reduced diversity and enrichment of pro-inflammatory taxa, is implicated in the pathogenesis of polycystic ovary syndrome (PCOS). Ramulus mori (Sangzhi) alkaloids (SZ-A), approved in China for type 2 diabetes with broad metabolic effects, remain untested as a microbiota-targeted intervention for PCOS.
METHODS: In a dehydroepiandrosterone (DHEA)-induced rat model of PCOS, we evaluated the therapeutic efficacy of SZ-A and its underlying microbiota-metabolite interactions through integrated assessments of reproductive and endocrine-metabolic function, oxidative stress, inflammatory cytokines, and gut microbiota and serum metabolite profiles.
RESULTS: Relative to SD rats, PCOS rats showed approximately 10-fold higher cystic follicle burden and a one-third reduction in corpora lutea, with serum testosterone rising from 0.12 ± 0.08 to 0.27 ± 0.08 ng/mL, total bile acids falling from 34.22 ± 5.52 to 20.63 ± 4.94 μM, and HOMA-IR significantly increased (all p < 0.05). SZ-A treatment reduced cystic follicles, restored estrous cyclicity and luteal formation, and shifted testosterone, total bile acids, and HOMA-IR toward SD levels. At the molecular level, SZ-A appears to act by remodeling gut microbiota composition and serum metabolite profiles. SZ-A significantly shifted microbial β-diversity in PCOS rats while retaining a community dominated by Bacteroidetes and Firmicutes with Lactobacillus and Treponema_2 as key genera. Untargeted metabolomics identified 13 PCOS-associated serum metabolites that were significantly reduced after SZ-A treatment (p < 0.05), highlighting fenoldopam as a putative mediator of its beneficial effects on ovarian function and metabolic homeostasis. With respect to oxidative injury, serum malondialdehyde (MDA) levels in PCOS rats were approximately twice those of the SD group, while total antioxidant capacity (T-AOC) and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were significantly reduced (p < 0.05); treatment with SZ-A markedly attenuated these alterations (p < 0.05). Besides, it suppressed systemic inflammation by reducing interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) levels in serum and relevant tissues (p < 0.05).
DISCUSSION: Collectively, these findings indicate that SZ-A alleviates PCOS by attenuating intestinal oxidative stress and normalizing gut microbiota-metabolite interactions, and highlight fenoldopam as a potential effector, supporting SZ-A as a promising therapeutic candidate for PCOS.},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Maternal Toxoplasma gondii Infection Perturbs Foetal and Maternal Foetal Interface Metabolism, Exposing the Foetus to Kynurenine.
British journal of biomedical science, 82:14989.
INTRODUCTION: Toxoplasma gondii infection during pregnancy can result in abortion or congenital infection. Events in the maternal-foetal interface, which form a selective barrier between the maternal and foetal circulations and where critical immunological adaptations occur, are critical in determining the pregnancy outcome. Recent studies have demonstrated that T. gondii infection can alter host metabolism, but how T. gondii infection alters the placenta or the foetus metabolome has not been reported.
METHODS: Herein, for the first time, we use liquid chromatography mass spectrometry (LCMS) in the BALB/c murine model of congenital T. gondii to address this shortcoming.
RESULTS: Maternal infection resulted in dysregulation of free amino acids with significant decreases in the levels of arginine, proline, threonine, methionine, leucine, glycine and glutamine detected in the decidua. Similar changes were noted in the placenta, although differences were less pronounced. In contrast, amino acid levels were not significantly altered in the foetal extracts. Results demonstrate that T. gondii infection induces the highest number of metabolite changes in the maternal serum. However, a subset of these changes was also found in the maternal-foetal interface and in the developing foetus. Maternal infection resulted in changes to arginine metabolism and downregulation of the urea cycle. Specifically, ornithine, arginosuccinate and citrulline were significantly decreased in all three tissues following maternal infection. Increased levels of spermidine were evident in the placenta and foetal extracts and not in the decidua from maternally infected mice. This indicates that maternal T. gondii infection downregulates the urea cycle, while increasing flux into polyamine biosynthesis in the decidua, placenta and foetus. Maternal infection resulted in an alteration to the tryptophan degradation pathway. Significantly decreased levels of kynurenine were seen in the decidua and placenta of maternally infected mice in comparison with the uninfected controls. In contrast, there was a significant increase in kynurenine in foetal extracts from maternally infected mice. Some metabolites from microbiome origin, including indoxylsulfate and 4-guanidinobutanoate, were changed compared with the controls, suggesting the potential of T. gondii to change the host microbiome.
DISCUSSION: The data presented herein demonstrate that T. gondii infection during pregnancy alters the metabolome of the maternal-foetal interface and developing foetus. Notably increased kynurenine and decreased tryptophan levels were found in the foetal tissue. As kynurenine is known to be produced during maternal immune activation and has been implicated in the development of psychoneurological diseases these changes could have important implications for the offspring over their lifetime.
Additional Links: PMID-41717231
PubMed:
Citation:
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@article {pmid41717231,
year = {2025},
author = {Arshad, H and Westrop, G and Teixeira, N and Borges, M and Roberts, CW},
title = {Maternal Toxoplasma gondii Infection Perturbs Foetal and Maternal Foetal Interface Metabolism, Exposing the Foetus to Kynurenine.},
journal = {British journal of biomedical science},
volume = {82},
number = {},
pages = {14989},
pmid = {41717231},
issn = {2474-0896},
mesh = {Female ; Animals ; Pregnancy ; *Toxoplasma/pathogenicity ; Mice ; *Kynurenine/metabolism ; *Placenta/metabolism/parasitology ; Mice, Inbred BALB C ; *Fetus/metabolism/parasitology ; *Toxoplasmosis/metabolism/parasitology ; *Maternal-Fetal Exchange ; *Pregnancy Complications, Parasitic/metabolism/parasitology ; *Toxoplasmosis, Animal/metabolism/parasitology ; Amino Acids/metabolism ; Disease Models, Animal ; },
abstract = {INTRODUCTION: Toxoplasma gondii infection during pregnancy can result in abortion or congenital infection. Events in the maternal-foetal interface, which form a selective barrier between the maternal and foetal circulations and where critical immunological adaptations occur, are critical in determining the pregnancy outcome. Recent studies have demonstrated that T. gondii infection can alter host metabolism, but how T. gondii infection alters the placenta or the foetus metabolome has not been reported.
METHODS: Herein, for the first time, we use liquid chromatography mass spectrometry (LCMS) in the BALB/c murine model of congenital T. gondii to address this shortcoming.
RESULTS: Maternal infection resulted in dysregulation of free amino acids with significant decreases in the levels of arginine, proline, threonine, methionine, leucine, glycine and glutamine detected in the decidua. Similar changes were noted in the placenta, although differences were less pronounced. In contrast, amino acid levels were not significantly altered in the foetal extracts. Results demonstrate that T. gondii infection induces the highest number of metabolite changes in the maternal serum. However, a subset of these changes was also found in the maternal-foetal interface and in the developing foetus. Maternal infection resulted in changes to arginine metabolism and downregulation of the urea cycle. Specifically, ornithine, arginosuccinate and citrulline were significantly decreased in all three tissues following maternal infection. Increased levels of spermidine were evident in the placenta and foetal extracts and not in the decidua from maternally infected mice. This indicates that maternal T. gondii infection downregulates the urea cycle, while increasing flux into polyamine biosynthesis in the decidua, placenta and foetus. Maternal infection resulted in an alteration to the tryptophan degradation pathway. Significantly decreased levels of kynurenine were seen in the decidua and placenta of maternally infected mice in comparison with the uninfected controls. In contrast, there was a significant increase in kynurenine in foetal extracts from maternally infected mice. Some metabolites from microbiome origin, including indoxylsulfate and 4-guanidinobutanoate, were changed compared with the controls, suggesting the potential of T. gondii to change the host microbiome.
DISCUSSION: The data presented herein demonstrate that T. gondii infection during pregnancy alters the metabolome of the maternal-foetal interface and developing foetus. Notably increased kynurenine and decreased tryptophan levels were found in the foetal tissue. As kynurenine is known to be produced during maternal immune activation and has been implicated in the development of psychoneurological diseases these changes could have important implications for the offspring over their lifetime.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Female
Animals
Pregnancy
*Toxoplasma/pathogenicity
Mice
*Kynurenine/metabolism
*Placenta/metabolism/parasitology
Mice, Inbred BALB C
*Fetus/metabolism/parasitology
*Toxoplasmosis/metabolism/parasitology
*Maternal-Fetal Exchange
*Pregnancy Complications, Parasitic/metabolism/parasitology
*Toxoplasmosis, Animal/metabolism/parasitology
Amino Acids/metabolism
Disease Models, Animal
RevDate: 2026-02-20
CmpDate: 2026-02-20
Spatiotemporal dynamics of rhizosphere microbial communities under different mulching methods in spring maize.
Frontiers in plant science, 17:1732283.
INTRODUCTION: Plastic film mulching is a critical practice in arid agroecosystems, yet its spatiotemporal impacts on the rhizosphere microbiome remain poorly understood.
METHODS: Here, we investigated how no-mulching (CK), on-film hole sowing (UPM), and film-side planting (FPM) shape the bacterial and fungal communities in the maize rhizosphere across developmental stages (V12 and R6) and soil depths (10, 20, and 30 cm).
RESULTS: Concurrently, both mulching strategies increased maize yield relative to CK, with FPM ultimately outperforming UPM (19.05% vs. 6.24%). Amplicon sequencing showed that mulching strongly structured the rhizosphere microbiome with clear spatiotemporal variation. Bacterial and fungal communities exhibited contrasting patterns: bacteria responded mainly in topsoil at V12 and across all depths by R6, whereas fungi responded across the soil profile at V12, with responses weakening with depth at R6. Mulching-particularly UPM-reduced key taxa, including the nitrifying genus Nitrospira and symbiotic Glomeromycota. Correlation analyses revealed significant associations between these taxonomic shifts and maize yield components, consistent with Nitrospira's preference for aerobic conditions. Functional predictions suggested UPM favored communities with higher representation of anaerobic decomposition pathways, whereas FPM supported greater potential for aerobic heterotrophy and nitrogen-related processes.
DISCUSSION: Although microbial shifts were correlated with yield components, yield increases were likely dominated by the direct physical effects of mulching. Overall, distinct mulching strategies generated divergent rhizosphere trajectories, with FPM potentially offering a more sustainable option for dryland maize production.
Additional Links: PMID-41717118
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@article {pmid41717118,
year = {2026},
author = {Wu, J and Chen, K and Sheng, L and Han, H and Li, J and Guo, Z and Gong, S and Wang, H and Chen, L and Zhang, Z and Gao, F},
title = {Spatiotemporal dynamics of rhizosphere microbial communities under different mulching methods in spring maize.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1732283},
pmid = {41717118},
issn = {1664-462X},
abstract = {INTRODUCTION: Plastic film mulching is a critical practice in arid agroecosystems, yet its spatiotemporal impacts on the rhizosphere microbiome remain poorly understood.
METHODS: Here, we investigated how no-mulching (CK), on-film hole sowing (UPM), and film-side planting (FPM) shape the bacterial and fungal communities in the maize rhizosphere across developmental stages (V12 and R6) and soil depths (10, 20, and 30 cm).
RESULTS: Concurrently, both mulching strategies increased maize yield relative to CK, with FPM ultimately outperforming UPM (19.05% vs. 6.24%). Amplicon sequencing showed that mulching strongly structured the rhizosphere microbiome with clear spatiotemporal variation. Bacterial and fungal communities exhibited contrasting patterns: bacteria responded mainly in topsoil at V12 and across all depths by R6, whereas fungi responded across the soil profile at V12, with responses weakening with depth at R6. Mulching-particularly UPM-reduced key taxa, including the nitrifying genus Nitrospira and symbiotic Glomeromycota. Correlation analyses revealed significant associations between these taxonomic shifts and maize yield components, consistent with Nitrospira's preference for aerobic conditions. Functional predictions suggested UPM favored communities with higher representation of anaerobic decomposition pathways, whereas FPM supported greater potential for aerobic heterotrophy and nitrogen-related processes.
DISCUSSION: Although microbial shifts were correlated with yield components, yield increases were likely dominated by the direct physical effects of mulching. Overall, distinct mulching strategies generated divergent rhizosphere trajectories, with FPM potentially offering a more sustainable option for dryland maize production.},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Convergent gut microbiome adaptation and pervasive antibiotic resistome in Qinghai-Tibet Plateau passerines.
Frontiers in microbiology, 16:1733974.
INTRODUCTION: The Qinghai-Tibet Plateau, an extreme high-altitude ecosystem, presents a unique model for studying host-microbe-environment coevolution under environmental stress. However, the role of resident wildlife, particularly non-migratory passerines, as reservoirs and vectors for cross-boundary antibiotic resistance gene (ARG) dissemination remains poorly understood.
METHODS: Here, through metagenomic analysis of two endemic passerines (Pseudopodoces humilis and Pyrgilauda ruficollis) and their habitats.
RESULTS: We reveal convergent adaptations in their gut microbiomes, dominated by Actinomycetota, Pseudomonadota and Bacillota. Functional enrichment in carbohydrate metabolism and genetic information processing underpins host energy optimization in extreme high-altitude environments. Critically, these birds constitute a major reservoir of ARGs, harboring 153 antibiotic resistance ontologies (AROs) with nearly universal resistance to clinical antibiotic classes. The core resistome-comprising glycopeptide (van clusters), fluoroquinolone, and tetracycline resistance genes-reflects anthropogenic contamination amplified by environmental persistence. Environmental transmission pathways were unequivocally demonstrated via 47 AROs shared between avian hosts and proximal matrices (soil/grass), coupled with livestock-derived antibiotic influx through excreta, establishing the plateau as a hotspot for resistance gene flux. Strikingly, "low-abundance-high-resistance" taxa (Pseudomonadota, Actinomycetota, and Bacillota; ≤30% abundance but >80% ARG contribution) drive resistome plasticity, potentially facilitated by horizontal gene transfer.
DISCUSSION: Our findings redefine resident passerines as sentinels of ecosystem health and bridges for cross-boundary antimicrobial resistance (AMR) spread. Mitigating global AMR thus necessitates interdisciplinary strategies targeting environmental reservoirs (e.g., regulating livestock antibiotic use) and monitoring avian-mediated gene flow.
Additional Links: PMID-41717089
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Citation:
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@article {pmid41717089,
year = {2025},
author = {Shi, S and Qi, J and Peng, W and Su, X and Chen, P and Xu, S and Li, S and Ma, L and Wang, W and Jiang, K and Liu, Z and Li, W and Xiong, H and Wang, Y},
title = {Convergent gut microbiome adaptation and pervasive antibiotic resistome in Qinghai-Tibet Plateau passerines.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1733974},
pmid = {41717089},
issn = {1664-302X},
abstract = {INTRODUCTION: The Qinghai-Tibet Plateau, an extreme high-altitude ecosystem, presents a unique model for studying host-microbe-environment coevolution under environmental stress. However, the role of resident wildlife, particularly non-migratory passerines, as reservoirs and vectors for cross-boundary antibiotic resistance gene (ARG) dissemination remains poorly understood.
METHODS: Here, through metagenomic analysis of two endemic passerines (Pseudopodoces humilis and Pyrgilauda ruficollis) and their habitats.
RESULTS: We reveal convergent adaptations in their gut microbiomes, dominated by Actinomycetota, Pseudomonadota and Bacillota. Functional enrichment in carbohydrate metabolism and genetic information processing underpins host energy optimization in extreme high-altitude environments. Critically, these birds constitute a major reservoir of ARGs, harboring 153 antibiotic resistance ontologies (AROs) with nearly universal resistance to clinical antibiotic classes. The core resistome-comprising glycopeptide (van clusters), fluoroquinolone, and tetracycline resistance genes-reflects anthropogenic contamination amplified by environmental persistence. Environmental transmission pathways were unequivocally demonstrated via 47 AROs shared between avian hosts and proximal matrices (soil/grass), coupled with livestock-derived antibiotic influx through excreta, establishing the plateau as a hotspot for resistance gene flux. Strikingly, "low-abundance-high-resistance" taxa (Pseudomonadota, Actinomycetota, and Bacillota; ≤30% abundance but >80% ARG contribution) drive resistome plasticity, potentially facilitated by horizontal gene transfer.
DISCUSSION: Our findings redefine resident passerines as sentinels of ecosystem health and bridges for cross-boundary antimicrobial resistance (AMR) spread. Mitigating global AMR thus necessitates interdisciplinary strategies targeting environmental reservoirs (e.g., regulating livestock antibiotic use) and monitoring avian-mediated gene flow.},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Epigenetic and microbiome responses to greens supplementation in obese older adults: results from a randomized crossover-controlled trial.
Frontiers in nutrition, 13:1750030.
Aging is influenced by genetic, environmental, and lifestyle factors. Preliminary studies suggest that fruit and vegetable-based dietary supplements may reduce inflammation and oxidative stress, key factors in aging. Greens-based supplements typically contain concentrated extracts of leafy greens, fruits, vegetables, and bioactive phytochemicals, providing micronutrients and polyphenols that may influence aging-related pathways. This exploratory study evaluated the effects of a 30-day greens-based supplement on epigenetic markers of aging and metabolic health in adults aged 50-65 years with body mass index (BMI) >30 kg/m[2], using a 60-day randomized crossover design. Participants were randomized to immediate or delayed supplementation. During the 30-day intervention period, participants consumed a daily greens supplement. Primary outcomes included peripheral blood mononuclear cell DNA methylation and epigenetic age (Horvath, PCGrimAge, AdaptAge, and DamAge). Secondary measures included clinical metabolic biomarkers, microbiome diversity, breath hydrogen and methane, body composition, actigraphy, dietary intake, and quality of life questionnaires [RAND 12 item short form questionnaire (SF-12), and 21-item Depression, Anxiety, and Stress Scale (DASS-21)]. Twenty-one participants began the protocol (65% female, mean age 58.4 ± 5.3 years, mean BMI 38.1 ± 8 kg/m[2]). Nineteen participants completed the study. Horvath clock data indicated that biological age paradoxically increased during the supplementation period, whereas newer-generation clocks (AdaptAge, DamAge) demonstrated trends toward improved outcomes. Gut microbiome alpha diversity remained stable; taxa of interest, including Bilophila (p = 0.037) and Desulfobacterota (p = 0.031) changed with supplementation. Body composition, metabolic biomarkers, dietary intake, breath gases, sleep, and psychosocial measures were unchanged during the study. Exploratory pre-to-post supplementation change score correlations found no significant associations between epigenetic clocks and secondary outcomes, except for an inverse relationship between Faith's phylogenetic diversity and fasting blood glucose (r s = -0.81, p < 0.001). In summary, 30 days of greens-based supplementation led to selective changes in epigenetic aging markers and individual gut microbial taxa, without significant effects on overall microbiome diversity, metabolic health markers, or body composition. Additionally, exploratory correlations suggest potential links between changes in microbial diversity and glycemic control following greens supplementation.
Additional Links: PMID-41717034
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Citation:
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@article {pmid41717034,
year = {2026},
author = {Robinson, LA and Cavanah, AM and Lennon, S and Mattingly, ML and Pol, WV and Huggins, KW and Greene, MW and Roberts, MD and Frugé, AD},
title = {Epigenetic and microbiome responses to greens supplementation in obese older adults: results from a randomized crossover-controlled trial.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1750030},
pmid = {41717034},
issn = {2296-861X},
abstract = {Aging is influenced by genetic, environmental, and lifestyle factors. Preliminary studies suggest that fruit and vegetable-based dietary supplements may reduce inflammation and oxidative stress, key factors in aging. Greens-based supplements typically contain concentrated extracts of leafy greens, fruits, vegetables, and bioactive phytochemicals, providing micronutrients and polyphenols that may influence aging-related pathways. This exploratory study evaluated the effects of a 30-day greens-based supplement on epigenetic markers of aging and metabolic health in adults aged 50-65 years with body mass index (BMI) >30 kg/m[2], using a 60-day randomized crossover design. Participants were randomized to immediate or delayed supplementation. During the 30-day intervention period, participants consumed a daily greens supplement. Primary outcomes included peripheral blood mononuclear cell DNA methylation and epigenetic age (Horvath, PCGrimAge, AdaptAge, and DamAge). Secondary measures included clinical metabolic biomarkers, microbiome diversity, breath hydrogen and methane, body composition, actigraphy, dietary intake, and quality of life questionnaires [RAND 12 item short form questionnaire (SF-12), and 21-item Depression, Anxiety, and Stress Scale (DASS-21)]. Twenty-one participants began the protocol (65% female, mean age 58.4 ± 5.3 years, mean BMI 38.1 ± 8 kg/m[2]). Nineteen participants completed the study. Horvath clock data indicated that biological age paradoxically increased during the supplementation period, whereas newer-generation clocks (AdaptAge, DamAge) demonstrated trends toward improved outcomes. Gut microbiome alpha diversity remained stable; taxa of interest, including Bilophila (p = 0.037) and Desulfobacterota (p = 0.031) changed with supplementation. Body composition, metabolic biomarkers, dietary intake, breath gases, sleep, and psychosocial measures were unchanged during the study. Exploratory pre-to-post supplementation change score correlations found no significant associations between epigenetic clocks and secondary outcomes, except for an inverse relationship between Faith's phylogenetic diversity and fasting blood glucose (r s = -0.81, p < 0.001). In summary, 30 days of greens-based supplementation led to selective changes in epigenetic aging markers and individual gut microbial taxa, without significant effects on overall microbiome diversity, metabolic health markers, or body composition. Additionally, exploratory correlations suggest potential links between changes in microbial diversity and glycemic control following greens supplementation.},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
The therapeutic potential of gypenosides for age-related macular degeneration.
Frontiers in nutrition, 13:1773391.
Additional Links: PMID-41717027
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@article {pmid41717027,
year = {2026},
author = {Cen, S and Li, J and Reilly, J and Chen, J and Jiang, HR and Shu, X},
title = {The therapeutic potential of gypenosides for age-related macular degeneration.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1773391},
pmid = {41717027},
issn = {2296-861X},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Root microbiome dynamics favor slow-growth strategies during Pinus seedling development.
ISME communications, 6(1):ycag018.
Microbial functional trait dynamics during seedling development-a critical yet underexplored driver of forest ecosystem establish, develop, and stability-remain poorly understood. We investigated bacterial genomic traits dynamics in subtropical Pinus massoniana seedlings over a growing season. Leaf-associated bacteria showed minimal temporal shifts, whereas root-associated bacteria exhibited pronounced trends: average genome size increased (independent of nitrogen addition), whereas ribosomal RNA operon copy number (RRN) declined under ambient nitrogen, indicating a transition from fast-growing to slow-growing strategies. These trajectories reflect the differential turnover of later, nitrogen-insensitive taxa (e.g. large-genome, low-RRN Bradyrhizobium) relative to earlier, nitrogen-sensitive taxa (e.g. small-genome, high-RRN Herbaspirillum) during colonization and establishment from an aerial source onto a developing host. Additionally, we detected a discrepancy between the temporal dynamics of predicted nitrogen fixation potential and quantitative real-time PCR-based nifH quantification, underscoring the need for caution when interpreting prediction-based functional potentials. These findings identify trait-mediated assembly as a key driver of early root microbiome dynamics in pine seedlings and highlight the need for temporally resolved, ground-truthed functional inference when predicting ecosystem processes.
Additional Links: PMID-41716870
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@article {pmid41716870,
year = {2026},
author = {Sun, C and Wang, C and Zhu, H and Chen, X and Chen, P and Li, Q and Gao, Z and Yang, B and Chen, L and Wang, N and Guo, L and Gao, C},
title = {Root microbiome dynamics favor slow-growth strategies during Pinus seedling development.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag018},
pmid = {41716870},
issn = {2730-6151},
abstract = {Microbial functional trait dynamics during seedling development-a critical yet underexplored driver of forest ecosystem establish, develop, and stability-remain poorly understood. We investigated bacterial genomic traits dynamics in subtropical Pinus massoniana seedlings over a growing season. Leaf-associated bacteria showed minimal temporal shifts, whereas root-associated bacteria exhibited pronounced trends: average genome size increased (independent of nitrogen addition), whereas ribosomal RNA operon copy number (RRN) declined under ambient nitrogen, indicating a transition from fast-growing to slow-growing strategies. These trajectories reflect the differential turnover of later, nitrogen-insensitive taxa (e.g. large-genome, low-RRN Bradyrhizobium) relative to earlier, nitrogen-sensitive taxa (e.g. small-genome, high-RRN Herbaspirillum) during colonization and establishment from an aerial source onto a developing host. Additionally, we detected a discrepancy between the temporal dynamics of predicted nitrogen fixation potential and quantitative real-time PCR-based nifH quantification, underscoring the need for caution when interpreting prediction-based functional potentials. These findings identify trait-mediated assembly as a key driver of early root microbiome dynamics in pine seedlings and highlight the need for temporally resolved, ground-truthed functional inference when predicting ecosystem processes.},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Maternal curcumin supplementation alleviates intestinal inflammation of Escherichia coli-infected offspring via modulating gut microbiome in chickens.
Animal nutrition (Zhongguo xu mu shou yi xue hui), 24:344-355.
The objective of this study was to investigate the effects of maternal curcumin (CUR) supplementation in breeder feed on the growth performance and intestinal health of offspring chickens infected with Escherichia coli. A total of 720 peak-laying Qingyuan partridge breeder hens at 28-week-old (initial body weight [IBW] 1950.11 ± 2.54 g) were fed either a basal diet, or a basal diet with 100, 200, or 400 mg/kg CUR for 20 weeks before collecting breeding eggs. After hatching, 360 one-d-old (IBW 34.03 ± 0.18 g) female offspring were divided into five subgroups (72 per each CUR treatment, and 144 for basal diet treatment): offspring of breeders whose mothers were fed the basal diet group (CON); offspring of breeders whose mothers fed a basal diet and challenged with E. coli group (EC); and offspring of breeders whose mothers fed the basal diets containing 100, 200, or 400 mg/kg CUR and challenged with E. coli group (CUR100E, CUR200E, or CUR400E). All the offspring treatments had 6 replicates of 12 chickens per replicate cage, and chickens bred for 3 weeks. The results indicated that maternal CUR supplementation resulted in a dose-dependent deposition primarily in the yolk. Maternal CUR supplementation (P < 0.001) relieved the offspring chickens' weight loss, increased feed conversion rate, and decreased average daily gain, intestinal morphological damage, and goblet cell injury. And maternal CUR supplementation changed in intestinal barrier genes (zonula occludens-1, occludin, and mucin 2), inflammatory factors (tumor necrosis factor α and interleukin-22), and oxidative markers (total antioxidant capacity and glutathione peroxidase) caused by E. coli infection (P < 0.05). Additionally, maternal CUR supplementation reversed the reduction in offspring chickens' gut microbial diversity (Shannon and Simpson indexes, P < 0.001) caused by E. coli infection. Maternal supplementation with CUR demonstrated a significant reduction in the colonization of Barnesiella (P < 0.001), which was found to have a positive correlation with intestinal inflammatory cytokines and oxidative stress. Concurrently, maternal CUR increased the relative abundance of Lactobacillus (P < 0.05), which was negatively correlated with intestinal inflammation and oxidative stress. The present study showed that maternal CUR supplementation can alleviate intestinal inflammation in offspring chickens, which may be mediated by regulating gut microbiota composition.
Additional Links: PMID-41716840
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@article {pmid41716840,
year = {2026},
author = {Xu, Y and Huang, Y and Zhu, Y and Wang, J and Elsenousey, HK and Fouad, AM and Lin, X and Zhang, S and Han, Y and Yan, S and Jiang, Z and Jiang, S and Ruan, D},
title = {Maternal curcumin supplementation alleviates intestinal inflammation of Escherichia coli-infected offspring via modulating gut microbiome in chickens.},
journal = {Animal nutrition (Zhongguo xu mu shou yi xue hui)},
volume = {24},
number = {},
pages = {344-355},
pmid = {41716840},
issn = {2405-6383},
abstract = {The objective of this study was to investigate the effects of maternal curcumin (CUR) supplementation in breeder feed on the growth performance and intestinal health of offspring chickens infected with Escherichia coli. A total of 720 peak-laying Qingyuan partridge breeder hens at 28-week-old (initial body weight [IBW] 1950.11 ± 2.54 g) were fed either a basal diet, or a basal diet with 100, 200, or 400 mg/kg CUR for 20 weeks before collecting breeding eggs. After hatching, 360 one-d-old (IBW 34.03 ± 0.18 g) female offspring were divided into five subgroups (72 per each CUR treatment, and 144 for basal diet treatment): offspring of breeders whose mothers were fed the basal diet group (CON); offspring of breeders whose mothers fed a basal diet and challenged with E. coli group (EC); and offspring of breeders whose mothers fed the basal diets containing 100, 200, or 400 mg/kg CUR and challenged with E. coli group (CUR100E, CUR200E, or CUR400E). All the offspring treatments had 6 replicates of 12 chickens per replicate cage, and chickens bred for 3 weeks. The results indicated that maternal CUR supplementation resulted in a dose-dependent deposition primarily in the yolk. Maternal CUR supplementation (P < 0.001) relieved the offspring chickens' weight loss, increased feed conversion rate, and decreased average daily gain, intestinal morphological damage, and goblet cell injury. And maternal CUR supplementation changed in intestinal barrier genes (zonula occludens-1, occludin, and mucin 2), inflammatory factors (tumor necrosis factor α and interleukin-22), and oxidative markers (total antioxidant capacity and glutathione peroxidase) caused by E. coli infection (P < 0.05). Additionally, maternal CUR supplementation reversed the reduction in offspring chickens' gut microbial diversity (Shannon and Simpson indexes, P < 0.001) caused by E. coli infection. Maternal supplementation with CUR demonstrated a significant reduction in the colonization of Barnesiella (P < 0.001), which was found to have a positive correlation with intestinal inflammatory cytokines and oxidative stress. Concurrently, maternal CUR increased the relative abundance of Lactobacillus (P < 0.05), which was negatively correlated with intestinal inflammation and oxidative stress. The present study showed that maternal CUR supplementation can alleviate intestinal inflammation in offspring chickens, which may be mediated by regulating gut microbiota composition.},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Genome-resolved metagenomics reveals gastrointestinal microbiome adaptations in sheep responding to fiber- and starch-rich diets.
Animal nutrition (Zhongguo xu mu shou yi xue hui), 24:233-245.
The gastrointestinal tract of ruminants hosts a specialized microbial ecosystem that has evolved to efficiently digest fiber. However, modern intensive farming practices, which often involve reduced dietary fiber and increased grain supplementation, are linked to metabolic disorders in ruminants. Despite this, the understanding of the taxonomic and functional adaptations of the gastrointestinal microbiome to dietary changes remains limited, largely due to the challenges in obtaining high-resolution characterization of microbial communities. This study employed genome-resolved metagenomics to examine how a starch-rich (SR) grain-based diet compares to a fiber-rich (FR) hay-based diet in shaping the composition and function of the gastrointestinal microbiome in the rumen, jejunum, and cecum of Hu sheep. A total of 10 sheep (approximately 180 d old, with a body weight of 25.6 ± 0.41 kg) were allocated to the 2 dietary groups (SR and FR groups) for a 28-d experimental period, and metagenomic sequencing was performed on digesta samples from different gastrointestinal regions. Using a representative microbial gene catalog (RGMGC) and 10,373 metagenome-assembled genomes from previous studies,microbial composition, strain-level diversity, and carbohydrate-active enzyme profiles at higher taxonomic and functional resolution were analyzed. The results showed that the transition from the FR diet to the SR diet significantly altered the fermentation patterns and the structure and function of the sheep gastrointestinal microbiota. Community analysis revealed microbial taxa such as Prevotella spp., Alistipes spp., RC9 spp., CAG-110 spp., and Akkermansia spp. with significantly altered abundances (P < 0.05), primarily associated with the reduced fiber content in the SR diet. Moreover, the gastrointestinal microbiome exhibited strain-level changes in carbohydrate degradation, leading to reduced metabolic functions necessary for fiber processing. Comparative genomics at the single-genome level pinpointed Prevotella as a core genus with strains showing significant functional differences, notably in the capacity to degrade plant polysaccharides. Overall, these findings provide new insights into microbial regulation of gastrointestinal health and offer valuable enzyme gene resources in ruminants.
Additional Links: PMID-41716833
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@article {pmid41716833,
year = {2026},
author = {Xie, F and Li, J and Liu, P and Xu, L and Wang, Y and Qiu, Q and Mao, S},
title = {Genome-resolved metagenomics reveals gastrointestinal microbiome adaptations in sheep responding to fiber- and starch-rich diets.},
journal = {Animal nutrition (Zhongguo xu mu shou yi xue hui)},
volume = {24},
number = {},
pages = {233-245},
pmid = {41716833},
issn = {2405-6383},
abstract = {The gastrointestinal tract of ruminants hosts a specialized microbial ecosystem that has evolved to efficiently digest fiber. However, modern intensive farming practices, which often involve reduced dietary fiber and increased grain supplementation, are linked to metabolic disorders in ruminants. Despite this, the understanding of the taxonomic and functional adaptations of the gastrointestinal microbiome to dietary changes remains limited, largely due to the challenges in obtaining high-resolution characterization of microbial communities. This study employed genome-resolved metagenomics to examine how a starch-rich (SR) grain-based diet compares to a fiber-rich (FR) hay-based diet in shaping the composition and function of the gastrointestinal microbiome in the rumen, jejunum, and cecum of Hu sheep. A total of 10 sheep (approximately 180 d old, with a body weight of 25.6 ± 0.41 kg) were allocated to the 2 dietary groups (SR and FR groups) for a 28-d experimental period, and metagenomic sequencing was performed on digesta samples from different gastrointestinal regions. Using a representative microbial gene catalog (RGMGC) and 10,373 metagenome-assembled genomes from previous studies,microbial composition, strain-level diversity, and carbohydrate-active enzyme profiles at higher taxonomic and functional resolution were analyzed. The results showed that the transition from the FR diet to the SR diet significantly altered the fermentation patterns and the structure and function of the sheep gastrointestinal microbiota. Community analysis revealed microbial taxa such as Prevotella spp., Alistipes spp., RC9 spp., CAG-110 spp., and Akkermansia spp. with significantly altered abundances (P < 0.05), primarily associated with the reduced fiber content in the SR diet. Moreover, the gastrointestinal microbiome exhibited strain-level changes in carbohydrate degradation, leading to reduced metabolic functions necessary for fiber processing. Comparative genomics at the single-genome level pinpointed Prevotella as a core genus with strains showing significant functional differences, notably in the capacity to degrade plant polysaccharides. Overall, these findings provide new insights into microbial regulation of gastrointestinal health and offer valuable enzyme gene resources in ruminants.},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Mycobiome dysbiosis and genetic predisposition to elevated IL-17A contribute to fibrosis in MASLD.
JHEP reports : innovation in hepatology, 8(3):101721.
BACKGROUND & AIMS: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the leading cause of chronic liver disease in Western countries. Progression to metabolic dysfunction-associated steatohepatitis (MASH) occurs when fat accumulation in the liver triggers inflammatory processes including T helper 17 cell (Th17) activation. We aimed to investigate the role of intestinal fungi in MASH-mediating Th17-associated signaling.
METHODS: Blood samples from patients with MASLD (n = 451), including 141 with histology-proven MASH, were genotyped for IL17A rs2275913. Microbiome composition was assessed by ITS1 and 16S rRNA sequencing of stool samples from patients with MASLD (n = 221), including 79 with histology-proven MASH, as well as 25 healthy controls. Highly abundant fungal species identified in patients with MASH were used to stimulate IL17A rs2275913-genotyped T cells ex vivo, and cytokine levels were measured (n = 9 per genotype). Th17/resting regulatory T cell (Th17/rTreg) ratios were analyzed in relation to IL17A rs2275913 genotype in patients with MASLD (n = 58), including 31 with histology-proven MASH, and 28 healthy controls.
RESULTS: We identified the IL17A rs2275913 minor allele variant as a risk factor for fibrosis progression in patients with MASLD. In patients with advanced fibrosis, we also observed an increased abundance of fungal CTG species, including Candida albicans and Debaryomyces hansenii, which are potent triggers of Th17 responses. Integrating genetic predisposition with mycobiome composition, ex vivo T-cell stimulation assays demonstrated that donors carrying the IL17A rs2275913 minor allele secreted significantly higher levels of IL-17A in response to CTG species. Additionally, patients with MASH carrying the IL17A rs2275913 risk allele had elevated Th17/Treg ratios in peripheral blood.
CONCLUSIONS: Genetic predisposition to enhanced Th17 responses, in the context of mycobiome dysbiosis, may promote MASH progression and liver fibrosis.
IMPACT AND IMPLICATIONS: Liver inflammation and fibrosis are key drivers of the transition from bland steatosis to metabolic dysfunction-associated steatohepatitis (MASH). Our findings identify a combinatorial mechanism in which genetic predisposition to enhanced IL-17A signaling, together with gut mycobiome dysbiosis, promotes MASH development and fibrosis progression. This work highlights the importance of host-mycobiome interactions in shaping inflammatory liver disease and supports further investigation into targeted strategies aimed at modulating IL-17A-mediated immune responses in patients with MASLD. Such approaches may offer novel opportunities for risk stratification and therapeutic intervention.
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@article {pmid41716747,
year = {2026},
author = {Thielemann, N and Siliceo, SL and Rau, M and Schöninger, A and Reus, N and Aldejohann, AM and Shehata, A and Behr, IS and Nieuwenhuizen, NE and Herz, M and Hermanns, HM and Mirhakkak, M and Löffler, J and Dandekar, T and Hünniger-Ast, K and Martin, R and Panagiotou, G and Geier, A and Kurzai, O},
title = {Mycobiome dysbiosis and genetic predisposition to elevated IL-17A contribute to fibrosis in MASLD.},
journal = {JHEP reports : innovation in hepatology},
volume = {8},
number = {3},
pages = {101721},
pmid = {41716747},
issn = {2589-5559},
abstract = {BACKGROUND & AIMS: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the leading cause of chronic liver disease in Western countries. Progression to metabolic dysfunction-associated steatohepatitis (MASH) occurs when fat accumulation in the liver triggers inflammatory processes including T helper 17 cell (Th17) activation. We aimed to investigate the role of intestinal fungi in MASH-mediating Th17-associated signaling.
METHODS: Blood samples from patients with MASLD (n = 451), including 141 with histology-proven MASH, were genotyped for IL17A rs2275913. Microbiome composition was assessed by ITS1 and 16S rRNA sequencing of stool samples from patients with MASLD (n = 221), including 79 with histology-proven MASH, as well as 25 healthy controls. Highly abundant fungal species identified in patients with MASH were used to stimulate IL17A rs2275913-genotyped T cells ex vivo, and cytokine levels were measured (n = 9 per genotype). Th17/resting regulatory T cell (Th17/rTreg) ratios were analyzed in relation to IL17A rs2275913 genotype in patients with MASLD (n = 58), including 31 with histology-proven MASH, and 28 healthy controls.
RESULTS: We identified the IL17A rs2275913 minor allele variant as a risk factor for fibrosis progression in patients with MASLD. In patients with advanced fibrosis, we also observed an increased abundance of fungal CTG species, including Candida albicans and Debaryomyces hansenii, which are potent triggers of Th17 responses. Integrating genetic predisposition with mycobiome composition, ex vivo T-cell stimulation assays demonstrated that donors carrying the IL17A rs2275913 minor allele secreted significantly higher levels of IL-17A in response to CTG species. Additionally, patients with MASH carrying the IL17A rs2275913 risk allele had elevated Th17/Treg ratios in peripheral blood.
CONCLUSIONS: Genetic predisposition to enhanced Th17 responses, in the context of mycobiome dysbiosis, may promote MASH progression and liver fibrosis.
IMPACT AND IMPLICATIONS: Liver inflammation and fibrosis are key drivers of the transition from bland steatosis to metabolic dysfunction-associated steatohepatitis (MASH). Our findings identify a combinatorial mechanism in which genetic predisposition to enhanced IL-17A signaling, together with gut mycobiome dysbiosis, promotes MASH development and fibrosis progression. This work highlights the importance of host-mycobiome interactions in shaping inflammatory liver disease and supports further investigation into targeted strategies aimed at modulating IL-17A-mediated immune responses in patients with MASLD. Such approaches may offer novel opportunities for risk stratification and therapeutic intervention.},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Corrigendum to 'The lung microbiome in patients with HIV complicated with community-acquired pneumonia: across-sectional pilot study' Current Research in Microbial Sciences Volume 9, 2025, 100480.
Current research in microbial sciences, 10:100537 pii:S2666-5174(25)00196-8.
[This corrects the article DOI: 10.1016/j.crmicr.2025.100480.].
Additional Links: PMID-41716697
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@article {pmid41716697,
year = {2026},
author = {Song, Y and Xu, X and Xie, M and Tao, J and Jin, H and Liu, Y and Liu, L and Song, X and Meng, S and Cheong, IH and Wang, Y and Wei, Q},
title = {Corrigendum to 'The lung microbiome in patients with HIV complicated with community-acquired pneumonia: across-sectional pilot study' Current Research in Microbial Sciences Volume 9, 2025, 100480.},
journal = {Current research in microbial sciences},
volume = {10},
number = {},
pages = {100537},
doi = {10.1016/j.crmicr.2025.100537},
pmid = {41716697},
issn = {2666-5174},
abstract = {[This corrects the article DOI: 10.1016/j.crmicr.2025.100480.].},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Structure and Spatial Heterogeneity of Chemosynthesis-Based Deep-Sea Archaeal and Bacterial Communities in Western South Atlantic.
Ecology and evolution, 16(2):e72973.
Cold seeps are widespread deep-sea ecosystems sustained by methane-rich fluid seepage and host dense chemosynthesis-based biological communities. In 2016, a methane-driven chemosynthetic system was discovered on the Rio Grande Cone, in the Western South Atlantic Ocean, but the structure and drivers of its prokaryotic communities remained poorly understood. Here, we investigated archaeal and bacterial communities associated with deep-sea sediments across three geographic areas (A, C, and E) and a vertical gradient of up to 18 m below the seafloor, encompassing sediment layers within and below the sulfate-methane transition zone (SMTZ). Community composition was assessed using high-throughput sequencing of the 16S rRNA gene (V3-V4 region), processed into amplicon sequence variants (ASVs), and related to local geochemical gradients using multivariate analyses. To disentangle the ecological responses of methane-cycling taxa from the broader microbiome, the prokaryotic community was analyzed by contrasting the ANME-SRB consortium with the remaining archaeal and bacterial taxa. Both groups exhibited significant spatial structuring across areas and sediment layers. Methane concentration and depth were the dominant drivers shaping both ANME-SRB and the remaining prokaryotic community, with conductivity further influencing the latter. Core microbiome analysis revealed a small number of widespread taxa accounting for a large proportion of total community abundance, including an atypical dominance of the archaeal genus Sulfophobococcus. Functional predictions indicated a predominance of sulfur- and nitrogen-related metabolisms, with no clear depth-structured metabolic profiles across the SMTZ. Overall, our results highlight how local geochemical gradients shape both methane-cycling and non-methane-cycling prokaryotic assemblages in a poorly explored South Atlantic cold seep, providing a baseline for future genome-resolved investigations of microbial functioning in this system.
Additional Links: PMID-41716592
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@article {pmid41716592,
year = {2026},
author = {Lopes Simão, TL and Felix Ribeiro, KA and Dias, R and Augustin, AH and Rodrigues, LF and Miller, DJ and Viana, AR and Triplett, EW and Ketzer, JMM and Giongo, A and Eizirik, E and Medina-Silva, R},
title = {Structure and Spatial Heterogeneity of Chemosynthesis-Based Deep-Sea Archaeal and Bacterial Communities in Western South Atlantic.},
journal = {Ecology and evolution},
volume = {16},
number = {2},
pages = {e72973},
pmid = {41716592},
issn = {2045-7758},
abstract = {Cold seeps are widespread deep-sea ecosystems sustained by methane-rich fluid seepage and host dense chemosynthesis-based biological communities. In 2016, a methane-driven chemosynthetic system was discovered on the Rio Grande Cone, in the Western South Atlantic Ocean, but the structure and drivers of its prokaryotic communities remained poorly understood. Here, we investigated archaeal and bacterial communities associated with deep-sea sediments across three geographic areas (A, C, and E) and a vertical gradient of up to 18 m below the seafloor, encompassing sediment layers within and below the sulfate-methane transition zone (SMTZ). Community composition was assessed using high-throughput sequencing of the 16S rRNA gene (V3-V4 region), processed into amplicon sequence variants (ASVs), and related to local geochemical gradients using multivariate analyses. To disentangle the ecological responses of methane-cycling taxa from the broader microbiome, the prokaryotic community was analyzed by contrasting the ANME-SRB consortium with the remaining archaeal and bacterial taxa. Both groups exhibited significant spatial structuring across areas and sediment layers. Methane concentration and depth were the dominant drivers shaping both ANME-SRB and the remaining prokaryotic community, with conductivity further influencing the latter. Core microbiome analysis revealed a small number of widespread taxa accounting for a large proportion of total community abundance, including an atypical dominance of the archaeal genus Sulfophobococcus. Functional predictions indicated a predominance of sulfur- and nitrogen-related metabolisms, with no clear depth-structured metabolic profiles across the SMTZ. Overall, our results highlight how local geochemical gradients shape both methane-cycling and non-methane-cycling prokaryotic assemblages in a poorly explored South Atlantic cold seep, providing a baseline for future genome-resolved investigations of microbial functioning in this system.},
}
RevDate: 2026-02-20
Editorial: New insights into gut microbiota in colorectal cancer.
Frontiers in cellular and infection microbiology, 16:1788000.
Additional Links: PMID-41716463
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@article {pmid41716463,
year = {2026},
author = {Kapur, N and Hassan, SA},
title = {Editorial: New insights into gut microbiota in colorectal cancer.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1788000},
doi = {10.3389/fcimb.2026.1788000},
pmid = {41716463},
issn = {2235-2988},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
The role of the microbial-immune-bone axis in bone tumor development: mechanistic integration, systems modeling, and intervention prospects.
Frontiers in cellular and infection microbiology, 16:1762046.
The emergence and development of bone tumors stem from a combination of intrinsic genetic alterations in tumor cells, remodeling of the bone marrow microenvironment, and shifts in the host's systemic immune-metabolic state. In recent years, gut microorganisms have been shown not only to influence bone mass regulation and conditions involving disrupted bone homeostasis, such as osteoporosis, but also to substantially affect the formation of primary bone tumors and metastatic lesions by modulating immune cell differentiation, inflammatory activity, and the coupling of bone remodeling. Focusing on the "Microbiota-Immune-Bone axis" (MIB), a growing body of fundamental and translational research indicates that alterations in gut microbial composition and function can reshape metabolite profiles-including short-chain fatty acids, bile acids, indole derivatives-and pathogen-associated molecular patterns (PAMPs). These signals act on the intestinal barrier and bone marrow immunity through G-protein-coupled receptors, nuclear receptors, and pattern-recognition receptors, thereby shifting the balance between bone resorption and formation and modifying the immune characteristics of the bone microenvironment, ultimately facilitating bone tumor cell colonization, proliferation, and immune escape. This review takes the MIB axis as its central framework to integrate the major pathways through which gut microbes and their metabolites regulate intestinal and myeloid immunity, bone remodeling, and bone tumor biology, to construct a systems-level model of tumor initiation and progression, to identify druggable signaling nodes, and to assess the potential and challenges of microbiota-modulating approaches-including antibiotics, probiotics, dietary strategies, and fecal microbiota transplantation-in preventing and treating bone tumors, thereby offering a theoretical foundation for developing integrated interventions targeting the gut microbiota and the MIB axis.
Additional Links: PMID-41716460
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Citation:
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@article {pmid41716460,
year = {2026},
author = {Guo, Y and Wang, X and Wu, Y and Li, Y and Wei, X},
title = {The role of the microbial-immune-bone axis in bone tumor development: mechanistic integration, systems modeling, and intervention prospects.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1762046},
pmid = {41716460},
issn = {2235-2988},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; Animals ; *Bone Neoplasms/immunology/pathology/microbiology ; Tumor Microenvironment/immunology ; *Bone and Bones/immunology/pathology ; Bone Remodeling ; },
abstract = {The emergence and development of bone tumors stem from a combination of intrinsic genetic alterations in tumor cells, remodeling of the bone marrow microenvironment, and shifts in the host's systemic immune-metabolic state. In recent years, gut microorganisms have been shown not only to influence bone mass regulation and conditions involving disrupted bone homeostasis, such as osteoporosis, but also to substantially affect the formation of primary bone tumors and metastatic lesions by modulating immune cell differentiation, inflammatory activity, and the coupling of bone remodeling. Focusing on the "Microbiota-Immune-Bone axis" (MIB), a growing body of fundamental and translational research indicates that alterations in gut microbial composition and function can reshape metabolite profiles-including short-chain fatty acids, bile acids, indole derivatives-and pathogen-associated molecular patterns (PAMPs). These signals act on the intestinal barrier and bone marrow immunity through G-protein-coupled receptors, nuclear receptors, and pattern-recognition receptors, thereby shifting the balance between bone resorption and formation and modifying the immune characteristics of the bone microenvironment, ultimately facilitating bone tumor cell colonization, proliferation, and immune escape. This review takes the MIB axis as its central framework to integrate the major pathways through which gut microbes and their metabolites regulate intestinal and myeloid immunity, bone remodeling, and bone tumor biology, to construct a systems-level model of tumor initiation and progression, to identify druggable signaling nodes, and to assess the potential and challenges of microbiota-modulating approaches-including antibiotics, probiotics, dietary strategies, and fecal microbiota transplantation-in preventing and treating bone tumors, thereby offering a theoretical foundation for developing integrated interventions targeting the gut microbiota and the MIB axis.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome/immunology
Animals
*Bone Neoplasms/immunology/pathology/microbiology
Tumor Microenvironment/immunology
*Bone and Bones/immunology/pathology
Bone Remodeling
RevDate: 2026-02-20
CmpDate: 2026-02-20
Chronic Antibiotic Use, Gut Microbiota Dysbiosis, and Increased Risk of Colorectal Cancer: An Emerging Threat.
Health science reports, 9(2):e71866.
BACKGROUND AND AIMS: The gut microbiota plays a vital role in host health by regulating metabolic processes, immune function, and epithelial barrier functions. Chronic use of antibiotics can alter this environment and introduce gut dysbiosis, which is defined as an alteration of microbial communities characterized by a loss of beneficial microbes and overgrowth of pathogenic microbes. Gut dysbiosis is increasingly associated with the development and progression of colorectal cancer (CRC). We explored the relationship between long-term antibiotic exposure, gut microbiota dysbiosis, and CRC risk, as well as strategies for preventing and restoring gut microbiomes.
METHODS: Relevant information was extracted from published articles available in PubMed, Scopus, and Google Scholar. The keywords "Gut," "Dysbiosis," "Antibiotic," "Colorectal," and "Microbiota" were used to search for relevant information.
RESULTS: Studies have demonstrated that chronic antibiotic exposure significantly reduces microbial diversity, particularly by decreasing beneficial species (e.g., Lactobacillus, Bifidobacterium, and Faecalibacterium), while favoring pathogenic species (e.g., Klebsiella pneumoniae and Enterococcus faecium). Antibiotic-induced dysbiosis reduces the production of microbial metabolites, including short-chain fatty acids, which are essential for supporting epithelial integrity and immune homeostasis. Prior antibiotic use is associated with a 13% increased risk of CRC, with antibiotic-induced microbiota alterations lasting for months to years. Several factors, including diet, pollution, and over-the-counter access to antibiotics in low-and middle-income countries, may contribute to an increased risk of dysbiosis and CRC. Additionally, interventions such as dietary fiber, probiotic supplementation, fecal microbiota transplantation, next-generation probiotics, and phage therapy may be potential strategies to restore the microbiome and achieve gut health.
CONCLUSION: Substantial use of antibiotics may alter the gut microbiota and increase the risk of CRC. To mitigate this risk, it is essential to practice prudent antibiotic use and adopt dietary, probiotic, and microbiome-restoring practices to support the health of the gut microbiome.
Additional Links: PMID-41716434
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Citation:
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@article {pmid41716434,
year = {2026},
author = {Mohiuddin, M},
title = {Chronic Antibiotic Use, Gut Microbiota Dysbiosis, and Increased Risk of Colorectal Cancer: An Emerging Threat.},
journal = {Health science reports},
volume = {9},
number = {2},
pages = {e71866},
pmid = {41716434},
issn = {2398-8835},
abstract = {BACKGROUND AND AIMS: The gut microbiota plays a vital role in host health by regulating metabolic processes, immune function, and epithelial barrier functions. Chronic use of antibiotics can alter this environment and introduce gut dysbiosis, which is defined as an alteration of microbial communities characterized by a loss of beneficial microbes and overgrowth of pathogenic microbes. Gut dysbiosis is increasingly associated with the development and progression of colorectal cancer (CRC). We explored the relationship between long-term antibiotic exposure, gut microbiota dysbiosis, and CRC risk, as well as strategies for preventing and restoring gut microbiomes.
METHODS: Relevant information was extracted from published articles available in PubMed, Scopus, and Google Scholar. The keywords "Gut," "Dysbiosis," "Antibiotic," "Colorectal," and "Microbiota" were used to search for relevant information.
RESULTS: Studies have demonstrated that chronic antibiotic exposure significantly reduces microbial diversity, particularly by decreasing beneficial species (e.g., Lactobacillus, Bifidobacterium, and Faecalibacterium), while favoring pathogenic species (e.g., Klebsiella pneumoniae and Enterococcus faecium). Antibiotic-induced dysbiosis reduces the production of microbial metabolites, including short-chain fatty acids, which are essential for supporting epithelial integrity and immune homeostasis. Prior antibiotic use is associated with a 13% increased risk of CRC, with antibiotic-induced microbiota alterations lasting for months to years. Several factors, including diet, pollution, and over-the-counter access to antibiotics in low-and middle-income countries, may contribute to an increased risk of dysbiosis and CRC. Additionally, interventions such as dietary fiber, probiotic supplementation, fecal microbiota transplantation, next-generation probiotics, and phage therapy may be potential strategies to restore the microbiome and achieve gut health.
CONCLUSION: Substantial use of antibiotics may alter the gut microbiota and increase the risk of CRC. To mitigate this risk, it is essential to practice prudent antibiotic use and adopt dietary, probiotic, and microbiome-restoring practices to support the health of the gut microbiome.},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Correction: Ramulus mori (Sangzhi) alkaloids improve intestinal oxidative damage and inflammation in DHEA-induced polycystic ovary syndrome rats via gut microbiota and metabolite modulation.
Frontiers in pharmacology, 17:1794631 pii:1794631.
[This corrects the article DOI: 10.3389/fphar.2025.1701694.].
Additional Links: PMID-41716311
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@article {pmid41716311,
year = {2026},
author = {Wang, Y and Jiang, X and Wu, S and Wang, Q and Zuo, D and Huang, B and Jian, L and Yang, Y and Cai, Y and Wen, X and Yao, L and Geng, S},
title = {Correction: Ramulus mori (Sangzhi) alkaloids improve intestinal oxidative damage and inflammation in DHEA-induced polycystic ovary syndrome rats via gut microbiota and metabolite modulation.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1794631},
doi = {10.3389/fphar.2026.1794631},
pmid = {41716311},
issn = {1663-9812},
abstract = {[This corrects the article DOI: 10.3389/fphar.2025.1701694.].},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Integrated multi-omics analysis reveals the involvement of the gut-brain axis in children with autism.
Frontiers in microbiology, 17:1766850.
BACKGROUND: Autism Spectrum Disorder (ASD) is frequently accompanied by gastrointestinal (GI) comorbidities and gut microbiota dysbiosis. While the microbiota-gut-brain axis is implicated in ASD pathophysiology, the upstream host genetic factors that drive these specific microbial alterations remain poorly characterized.
METHODS: To bridge this gap, we performed an integrated multi-omics analysis combining whole-exome sequencing, 16S rRNA gene sequencing, and plasma metabolomics in a cohort of children with ASD and typically developing controls.
RESULTS: We confirmed that children with ASD exhibit significant gut microbial dysbiosis and metabolic perturbations, which correlated with GI symptom severity. Crucially, rare variant enrichment analysis identified a significant accumulation of deleterious variants in mucin biosynthesis pathways (specifically the MUC gene family), which are essential for intestinal mucus barrier integrity. Multi-omics integration revealed that these host genetic defects were associated with distinct shifts in the gut ecosystem, notably the depletion of beneficial butyrate-producing bacteria (e.g., Faecalibacterium) and the expansion of mucin-degrading taxa. This structural dysbiosis translated into functional metabolic impairments, particularly in lipid transport and short-chain fatty acid metabolism, which tracked with ASD severity.
CONCLUSION: Collectively, our data argue for a host-centric cascade where genetic vulnerabilities-specifically within the MUC pathway-compromise mucosal integrity, acting as a selective filter that fundamentally reshapes the gut microbiome. By pinpointing these variants as upstream drivers of gut-brain axis dysfunction, we move beyond simple association to identify concrete genetic targets-rare deleterious variants in the mucin (MUC) gene family-for future precision interventions in ASD.
Additional Links: PMID-41716284
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@article {pmid41716284,
year = {2026},
author = {Zhong, H and Zhang, S and Mou, Z and Fan, X and Zhang, X and Wang, L and Xu, X and Xue, X and Yang, F and Shu, J and Wang, M and Cai, C},
title = {Integrated multi-omics analysis reveals the involvement of the gut-brain axis in children with autism.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1766850},
pmid = {41716284},
issn = {1664-302X},
abstract = {BACKGROUND: Autism Spectrum Disorder (ASD) is frequently accompanied by gastrointestinal (GI) comorbidities and gut microbiota dysbiosis. While the microbiota-gut-brain axis is implicated in ASD pathophysiology, the upstream host genetic factors that drive these specific microbial alterations remain poorly characterized.
METHODS: To bridge this gap, we performed an integrated multi-omics analysis combining whole-exome sequencing, 16S rRNA gene sequencing, and plasma metabolomics in a cohort of children with ASD and typically developing controls.
RESULTS: We confirmed that children with ASD exhibit significant gut microbial dysbiosis and metabolic perturbations, which correlated with GI symptom severity. Crucially, rare variant enrichment analysis identified a significant accumulation of deleterious variants in mucin biosynthesis pathways (specifically the MUC gene family), which are essential for intestinal mucus barrier integrity. Multi-omics integration revealed that these host genetic defects were associated with distinct shifts in the gut ecosystem, notably the depletion of beneficial butyrate-producing bacteria (e.g., Faecalibacterium) and the expansion of mucin-degrading taxa. This structural dysbiosis translated into functional metabolic impairments, particularly in lipid transport and short-chain fatty acid metabolism, which tracked with ASD severity.
CONCLUSION: Collectively, our data argue for a host-centric cascade where genetic vulnerabilities-specifically within the MUC pathway-compromise mucosal integrity, acting as a selective filter that fundamentally reshapes the gut microbiome. By pinpointing these variants as upstream drivers of gut-brain axis dysfunction, we move beyond simple association to identify concrete genetic targets-rare deleterious variants in the mucin (MUC) gene family-for future precision interventions in ASD.},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Interactions of bile acids and gut microbiota modulate neurological health: a comprehensive review on mechanisms and therapeutic potential of dietary phytochemicals.
Frontiers in microbiology, 17:1757551.
Bile acids (BAs), classically regarded as detergents for dietary lipid absorption, have emerged as pivotal signaling molecules with systemic endocrine functions. The discovery of the Farnesoid X Receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5) as BAs-activated receptors unveiled their profound influences on glucose, lipid, and energy metabolism. BAs are first synthesized in hepatocytes and further metabolized by gut microbes, can either circulate in enterohepatic system or be found in circulations to exert various effects. More recently, the gut-brain axis has been identified as a critical pathway through which BAs exert significant effects on central nervous system (CNS) function and health. Based on research progresses mentioned above, this review systematically delineates the synthesis, metabolism, and classification of BAs, with a focus on the intricate crosstalk between the hepatic-gut BA axis and the brain. In addition, we explore the compelling evidences linking BAs dysregulation to a spectrum of neurological disorders, including neurodegenerative diseases (Alzheimer's and Parkinson's disease), depression, and hepatic encephalopathy. Besides, the potential mechanisms, such as alleviating neuroinflammation, maintaining the integrity of blood-brain barrier, increasing the neuronal survival, and modulating neurotransmitter systems are further elucidated. Finally, strategies of dietary intervention through phytochemicals to modulate the BAs pool for improved neurological outcomes are summarized and discussed. By integrating pre-clinical and clinical findings, this review aims to establish a foundation for understanding BAs as novel therapeutic targets in neurology and nutritional neuroscience.
Additional Links: PMID-41716273
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Citation:
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@article {pmid41716273,
year = {2026},
author = {Wang, J and Zhang, Y and Wu, Q and Zhong, Y and Xu, Z and Yang, J},
title = {Interactions of bile acids and gut microbiota modulate neurological health: a comprehensive review on mechanisms and therapeutic potential of dietary phytochemicals.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1757551},
pmid = {41716273},
issn = {1664-302X},
abstract = {Bile acids (BAs), classically regarded as detergents for dietary lipid absorption, have emerged as pivotal signaling molecules with systemic endocrine functions. The discovery of the Farnesoid X Receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5) as BAs-activated receptors unveiled their profound influences on glucose, lipid, and energy metabolism. BAs are first synthesized in hepatocytes and further metabolized by gut microbes, can either circulate in enterohepatic system or be found in circulations to exert various effects. More recently, the gut-brain axis has been identified as a critical pathway through which BAs exert significant effects on central nervous system (CNS) function and health. Based on research progresses mentioned above, this review systematically delineates the synthesis, metabolism, and classification of BAs, with a focus on the intricate crosstalk between the hepatic-gut BA axis and the brain. In addition, we explore the compelling evidences linking BAs dysregulation to a spectrum of neurological disorders, including neurodegenerative diseases (Alzheimer's and Parkinson's disease), depression, and hepatic encephalopathy. Besides, the potential mechanisms, such as alleviating neuroinflammation, maintaining the integrity of blood-brain barrier, increasing the neuronal survival, and modulating neurotransmitter systems are further elucidated. Finally, strategies of dietary intervention through phytochemicals to modulate the BAs pool for improved neurological outcomes are summarized and discussed. By integrating pre-clinical and clinical findings, this review aims to establish a foundation for understanding BAs as novel therapeutic targets in neurology and nutritional neuroscience.},
}
RevDate: 2026-02-20
CmpDate: 2026-02-20
Comprehensive identification of contagious, environmental, and emerging microorganisms associated with bovine mastitis in Northern Minas Gerais, Brazil, using MALDI-TOF mass spectrometry.
Veterinary world, 18(12):4196-4211.
BACKGROUND AND AIM: Bovine mastitis remains one of the most economically significant diseases in dairy herds, driven by diverse etiological agents that vary in prevalence across regions and production systems. Rapid and reliable identification of mastitis-causing microorganisms is essential for targeted treatment, improved herd management, and enhanced biosecurity. This study aimed to identify and characterize the microorganisms associated with clinical and subclinical mastitis in dairy cows from northern Minas Gerais (Brazil) using Matrix-assisted laser desorption/ionization-time-of-flight mass spectrometry (MALDI-TOF MS), with special emphasis on uncommon and emerging bacterial species of potential public health concern.
MATERIALS AND METHODS: Milk samples (n = 321 isolates) were collected from cows diagnosed with clinical or subclinical mastitis between 2022 and 2024 across 15 farms. Bacteria were cultured on 5% sheep blood agar and identified by MALDI-TOF MS according to Bruker scoring criteria. Gram classification and contagious versus environmental categorization were performed. Descriptive statistics, chi-square analysis (p < 0.05), and Bray-Curtis similarity with Unweighted Pair Group Mathematical Average clustering were applied to determine distribution patterns and microbial diversity.
RESULTS: MALDI-TOF MS achieved an identification rate of 88%, predominantly at the species-level (99.38%). Gram-positive bacteria were significantly more frequent than Gram-negative bacteria (78%; χ² = 168.52; p < 0.000001). Most pathogens were classified as contagious (65%), followed by environmental agents (23%) (χ² = 64.40; p < 0.000001). The most prevalent organisms were Staphylococcus aureus (30.2%), Staphylococcus chromogenes (22.1%), and Sthaphylococcus epidermidis (4.9%). A combined frequency of 7.48% represented uncommon microorganisms, including Burkholderia cepacia, Arthrobacter koreensis, Ralstonia pickettii, Kosakonia radicincitans, Rothia terrae, and Paenibacillus azoreducens, some of which may pose emerging risks to bovine health and public health. Cluster analysis revealed two major microbial groups with distinct ecological and pathogenic profiles, highlighting the complexity of mastitis epidemiology in the region.
CONCLUSION: This study provides an updated and region-specific overview of the mastitis microbiome in northern Minas Gerais, demonstrating the predominance of S. aureus and non-aureus staphylococci, alongside diverse environmental and rare pathogens. MALDI-TOF MS proved to be a powerful diagnostic tool for rapid species-level identification, supporting more precise mastitis control strategies. The detection of emerging or uncommon microorganisms underscores the need for sustained surveillance, improved biosecurity, and further research, including genomic characterization and antimicrobial resistance monitoring. These findings contribute to advancing dairy herd health, guiding targeted interventions, and informing One Health perspectives.
Additional Links: PMID-41716168
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Citation:
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@article {pmid41716168,
year = {2025},
author = {Santos, EMS and de Souza, CN and Santos, HO and da Silva, LMV and Souza, GAAD and Oliveira, LF and Magalhães, MJR and Dos Santos, WS and Tavares, AMF and Ferreira, RGC and de Almeida, AC},
title = {Comprehensive identification of contagious, environmental, and emerging microorganisms associated with bovine mastitis in Northern Minas Gerais, Brazil, using MALDI-TOF mass spectrometry.},
journal = {Veterinary world},
volume = {18},
number = {12},
pages = {4196-4211},
pmid = {41716168},
issn = {0972-8988},
abstract = {BACKGROUND AND AIM: Bovine mastitis remains one of the most economically significant diseases in dairy herds, driven by diverse etiological agents that vary in prevalence across regions and production systems. Rapid and reliable identification of mastitis-causing microorganisms is essential for targeted treatment, improved herd management, and enhanced biosecurity. This study aimed to identify and characterize the microorganisms associated with clinical and subclinical mastitis in dairy cows from northern Minas Gerais (Brazil) using Matrix-assisted laser desorption/ionization-time-of-flight mass spectrometry (MALDI-TOF MS), with special emphasis on uncommon and emerging bacterial species of potential public health concern.
MATERIALS AND METHODS: Milk samples (n = 321 isolates) were collected from cows diagnosed with clinical or subclinical mastitis between 2022 and 2024 across 15 farms. Bacteria were cultured on 5% sheep blood agar and identified by MALDI-TOF MS according to Bruker scoring criteria. Gram classification and contagious versus environmental categorization were performed. Descriptive statistics, chi-square analysis (p < 0.05), and Bray-Curtis similarity with Unweighted Pair Group Mathematical Average clustering were applied to determine distribution patterns and microbial diversity.
RESULTS: MALDI-TOF MS achieved an identification rate of 88%, predominantly at the species-level (99.38%). Gram-positive bacteria were significantly more frequent than Gram-negative bacteria (78%; χ² = 168.52; p < 0.000001). Most pathogens were classified as contagious (65%), followed by environmental agents (23%) (χ² = 64.40; p < 0.000001). The most prevalent organisms were Staphylococcus aureus (30.2%), Staphylococcus chromogenes (22.1%), and Sthaphylococcus epidermidis (4.9%). A combined frequency of 7.48% represented uncommon microorganisms, including Burkholderia cepacia, Arthrobacter koreensis, Ralstonia pickettii, Kosakonia radicincitans, Rothia terrae, and Paenibacillus azoreducens, some of which may pose emerging risks to bovine health and public health. Cluster analysis revealed two major microbial groups with distinct ecological and pathogenic profiles, highlighting the complexity of mastitis epidemiology in the region.
CONCLUSION: This study provides an updated and region-specific overview of the mastitis microbiome in northern Minas Gerais, demonstrating the predominance of S. aureus and non-aureus staphylococci, alongside diverse environmental and rare pathogens. MALDI-TOF MS proved to be a powerful diagnostic tool for rapid species-level identification, supporting more precise mastitis control strategies. The detection of emerging or uncommon microorganisms underscores the need for sustained surveillance, improved biosecurity, and further research, including genomic characterization and antimicrobial resistance monitoring. These findings contribute to advancing dairy herd health, guiding targeted interventions, and informing One Health perspectives.},
}
RevDate: 2026-02-20
Skin deep: dermatologic challenges in PCOS through the female lifespan.
Expert review of endocrinology & metabolism [Epub ahead of print].
INTRODUCTION: Polycystic ovary syndrome (PCOS) is a lifelong endocrine-metabolic condition with prominent dermatologic manifestations such as hirsutism, acne/seborrhea, and female pattern hair loss (FPHL), which are frequently the initial complaint for seeking medical attention.
AREAS COVERED: This review explores the pathogenesis and dermatologic presentation of PCOS across the lifespan, emphasizing evidence-based diagnostic strategies, based on a PubMed literature search through August 2025. It also highlights the impact on quality of life, the need for psychosocial support, and the importance of cultural sensitivity in care. Management approaches are reviewed including pharmacologic therapies, procedures, and considerations across reproductive stages including pregnancy, postpartum, and menopause. Future directions in management are also discussed.
EXPERT OPINION: Current care remains largely symptom-driven. A shift toward mechanism-based, personalized therapy is essential. Key priorities include biomarker-guided treatment, standardized assessment tools, cautious antibiotic use with microbiome-sparing approaches, and clinical trials targeting treatment-resistant/recurrent cases and FPHL. In the future, routine care should incorporate phenotype- and biomarker-based algorithms, artificial intelligence (AI)-assisted assessment, and integrated mental health support.
Additional Links: PMID-41715888
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@article {pmid41715888,
year = {2026},
author = {Oğuz, SH and Yalici Armagan, B and Okan Yildiz, B},
title = {Skin deep: dermatologic challenges in PCOS through the female lifespan.},
journal = {Expert review of endocrinology & metabolism},
volume = {},
number = {},
pages = {1-20},
doi = {10.1080/17446651.2026.2632020},
pmid = {41715888},
issn = {1744-8417},
abstract = {INTRODUCTION: Polycystic ovary syndrome (PCOS) is a lifelong endocrine-metabolic condition with prominent dermatologic manifestations such as hirsutism, acne/seborrhea, and female pattern hair loss (FPHL), which are frequently the initial complaint for seeking medical attention.
AREAS COVERED: This review explores the pathogenesis and dermatologic presentation of PCOS across the lifespan, emphasizing evidence-based diagnostic strategies, based on a PubMed literature search through August 2025. It also highlights the impact on quality of life, the need for psychosocial support, and the importance of cultural sensitivity in care. Management approaches are reviewed including pharmacologic therapies, procedures, and considerations across reproductive stages including pregnancy, postpartum, and menopause. Future directions in management are also discussed.
EXPERT OPINION: Current care remains largely symptom-driven. A shift toward mechanism-based, personalized therapy is essential. Key priorities include biomarker-guided treatment, standardized assessment tools, cautious antibiotic use with microbiome-sparing approaches, and clinical trials targeting treatment-resistant/recurrent cases and FPHL. In the future, routine care should incorporate phenotype- and biomarker-based algorithms, artificial intelligence (AI)-assisted assessment, and integrated mental health support.},
}
RevDate: 2026-02-22
CmpDate: 2026-02-20
Paired Duodenal and Salivary Microbiome Analysis in Pancreatic Cancer Without Duct Obstruction.
United European gastroenterology journal, 14(2):e70179.
BACKGROUND: Bacterial migration from the oral cavity to the upper gastrointestinal tract has been proposed as a contributor to pancreatic ductal adenocarcinoma (PDAC) onset and prognosis. Whether PDAC is associated with alterations of the oral-duodenal microbiome continuum remains unclear.
METHODS: In this prospective study, we profiled matched saliva and duodenal brushings from 24 treatment-naïve PDAC patients without ducts obstruction and 24 age- and sex-matched healthy controls (HC). Microbial composition was assessed by 16S rRNA gene sequencing. α-Diversity was evaluated using Faith's phylogenetic diversity (PD), observed ASVs, and Pielou's evenness; β-diversity using UniFrac, Bray-Curtis, and distance-based redundancy analysis (db-RDA). Associations with overall survival were examined using Cox models and ROC-derived cut-offs, with leave-one-out cross-validation for robustness.
RESULTS: Duodenal Faith's PD was significantly lower in PDAC than HC (q = 0.034), whereas richness and evenness did not differ; no α-diversity differences were observed in saliva. After adjustment for diabetes and periodontitis, lower duodenal Faith's PD (q = 0.048) and ASV richness (q = 0.030) in PDAC remained significant. β-Diversity was primarily driven by body site, but adjusted db-RDA revealed a small yet significant PDAC-HC difference in duodenal community composition (pseudo-F = 2.16, p = 0.002). Several genera showed differential abundance between groups. Higher salivary phylogenetic diversity predicted longer survival (aHR = 0.19, p = 0.001), along with specific genera associated with favourable prognosis.
DISCUSSION: PDAC is associated with reduced duodenal phylogenetic diversity and subtle disease-related shifts in duodenal microbiota, independent of major confounders and in the absence of duct obstruction. Both α-diversity and selected genera may hold prognostic relevance, supporting further validation in larger, stage-stratified cohorts.
Additional Links: PMID-41715273
PubMed:
Citation:
show bibtex listing
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@article {pmid41715273,
year = {2026},
author = {Archibugi, L and Bertoldi, L and Benvenuto, G and Sattin, E and Ponz De Leon Pisani, R and Fortunato, C and Mariani, A and Rossi, G and Petrone, MC and Valle, G and Reni, M and Falconi, M and Arcidiacono, PG and Capurso, G},
title = {Paired Duodenal and Salivary Microbiome Analysis in Pancreatic Cancer Without Duct Obstruction.},
journal = {United European gastroenterology journal},
volume = {14},
number = {2},
pages = {e70179},
pmid = {41715273},
issn = {2050-6414},
support = {IG 26201//Associazione Italiana Ricerca Cancro/ ; IG 2015 17177//Associazione Italiana Ricerca Cancro/ ; },
mesh = {Humans ; *Saliva/microbiology ; Female ; Male ; *Pancreatic Neoplasms/microbiology/mortality/pathology ; Middle Aged ; *Duodenum/microbiology ; *Carcinoma, Pancreatic Ductal/microbiology/mortality/pathology ; Aged ; Prospective Studies ; RNA, Ribosomal, 16S/genetics ; Case-Control Studies ; Prognosis ; *Microbiota ; *Gastrointestinal Microbiome ; Phylogeny ; },
abstract = {BACKGROUND: Bacterial migration from the oral cavity to the upper gastrointestinal tract has been proposed as a contributor to pancreatic ductal adenocarcinoma (PDAC) onset and prognosis. Whether PDAC is associated with alterations of the oral-duodenal microbiome continuum remains unclear.
METHODS: In this prospective study, we profiled matched saliva and duodenal brushings from 24 treatment-naïve PDAC patients without ducts obstruction and 24 age- and sex-matched healthy controls (HC). Microbial composition was assessed by 16S rRNA gene sequencing. α-Diversity was evaluated using Faith's phylogenetic diversity (PD), observed ASVs, and Pielou's evenness; β-diversity using UniFrac, Bray-Curtis, and distance-based redundancy analysis (db-RDA). Associations with overall survival were examined using Cox models and ROC-derived cut-offs, with leave-one-out cross-validation for robustness.
RESULTS: Duodenal Faith's PD was significantly lower in PDAC than HC (q = 0.034), whereas richness and evenness did not differ; no α-diversity differences were observed in saliva. After adjustment for diabetes and periodontitis, lower duodenal Faith's PD (q = 0.048) and ASV richness (q = 0.030) in PDAC remained significant. β-Diversity was primarily driven by body site, but adjusted db-RDA revealed a small yet significant PDAC-HC difference in duodenal community composition (pseudo-F = 2.16, p = 0.002). Several genera showed differential abundance between groups. Higher salivary phylogenetic diversity predicted longer survival (aHR = 0.19, p = 0.001), along with specific genera associated with favourable prognosis.
DISCUSSION: PDAC is associated with reduced duodenal phylogenetic diversity and subtle disease-related shifts in duodenal microbiota, independent of major confounders and in the absence of duct obstruction. Both α-diversity and selected genera may hold prognostic relevance, supporting further validation in larger, stage-stratified cohorts.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Saliva/microbiology
Female
Male
*Pancreatic Neoplasms/microbiology/mortality/pathology
Middle Aged
*Duodenum/microbiology
*Carcinoma, Pancreatic Ductal/microbiology/mortality/pathology
Aged
Prospective Studies
RNA, Ribosomal, 16S/genetics
Case-Control Studies
Prognosis
*Microbiota
*Gastrointestinal Microbiome
Phylogeny
RevDate: 2026-02-22
CmpDate: 2026-02-20
Ecological insights into the cross-domain microbiome interactions in the hematophagous bat Desmodus rotundus.
Animal microbiome, 8(1):22.
BACKGROUND: Bats are recognised as reservoirs for a wide range of microorganisms, including viruses, bacteria, fungi, and parasites, some of which are of zoonotic concern. The common vampire bat (Desmodus rotundus) is particularly important due to its hematophagous feeding behaviour and ecological adaptability, both of which enhance its potential for cross-species pathogen transmission. Despite its well-established relevance to public health, the microbial communities associated with D. rotundus remain poorly characterised. This study aimed at investigating the composition, diversity, and interactions of prokaryotic, eukaryotic, and viral communities, alongside feeding sources, using high-throughput sequencing in 27 D. rotundus individuals from a rural area in Casanare, eastern Colombia.
RESULTS: We analysed a total of 81 samples (blood, faeces, and oral swabs) using long-read amplicon sequencing of the 16S- and 18S-rRNA genes and viral metagenomics via Oxford Nanopore Technologies. The microbial profiles revealed highly diverse assemblages, encompassing a wide range of bacterial, fungal, eukaryotic parasites, and viral taxa, with significant variation in community structure and diversity metrics across the three sample types collected from each bat. Taxa of public health concern were detected, including Enterococcus faecalis, Mycoplasma spp. Acanthamoeba spp. and viruses from the families Coronaviridae, Retroviridae, and Circoviridae. Correlation analyses suggested potential intra- and inter-domain interactions and co-occurrence dynamics among these microbes. Additionally, feeding source profiling, based on vertebrate assignments from faeces and swab samples, indicated evidence of livestock consumption, suggesting possible transmission pathways between bats and domestic animals.
CONCLUSIONS: The detection of multiple co-occurring pathogens across distinct sample types, coupled with their association with feeding sources, highlights the role of D. rotundus as a functionally specialised reservoir capable of harbouring and potentially disseminating zoonotic microbes. This study provides new insights into the cross-domain microbial ecology of hematophagous bats and underscores the need to integrate microbial community profiling with host behavioural data to enhance surveillance and mitigation strategies for zoonotic disease transmission.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s42523-025-00504-x.
Additional Links: PMID-41715245
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41715245,
year = {2026},
author = {Luna, N and Hernández, C and Ramírez, AL and Urbano, P and Barragán, K and Ariza, C and Muñoz, M and Patiño, LH and Ramírez, JD},
title = {Ecological insights into the cross-domain microbiome interactions in the hematophagous bat Desmodus rotundus.},
journal = {Animal microbiome},
volume = {8},
number = {1},
pages = {22},
pmid = {41715245},
issn = {2524-4671},
abstract = {BACKGROUND: Bats are recognised as reservoirs for a wide range of microorganisms, including viruses, bacteria, fungi, and parasites, some of which are of zoonotic concern. The common vampire bat (Desmodus rotundus) is particularly important due to its hematophagous feeding behaviour and ecological adaptability, both of which enhance its potential for cross-species pathogen transmission. Despite its well-established relevance to public health, the microbial communities associated with D. rotundus remain poorly characterised. This study aimed at investigating the composition, diversity, and interactions of prokaryotic, eukaryotic, and viral communities, alongside feeding sources, using high-throughput sequencing in 27 D. rotundus individuals from a rural area in Casanare, eastern Colombia.
RESULTS: We analysed a total of 81 samples (blood, faeces, and oral swabs) using long-read amplicon sequencing of the 16S- and 18S-rRNA genes and viral metagenomics via Oxford Nanopore Technologies. The microbial profiles revealed highly diverse assemblages, encompassing a wide range of bacterial, fungal, eukaryotic parasites, and viral taxa, with significant variation in community structure and diversity metrics across the three sample types collected from each bat. Taxa of public health concern were detected, including Enterococcus faecalis, Mycoplasma spp. Acanthamoeba spp. and viruses from the families Coronaviridae, Retroviridae, and Circoviridae. Correlation analyses suggested potential intra- and inter-domain interactions and co-occurrence dynamics among these microbes. Additionally, feeding source profiling, based on vertebrate assignments from faeces and swab samples, indicated evidence of livestock consumption, suggesting possible transmission pathways between bats and domestic animals.
CONCLUSIONS: The detection of multiple co-occurring pathogens across distinct sample types, coupled with their association with feeding sources, highlights the role of D. rotundus as a functionally specialised reservoir capable of harbouring and potentially disseminating zoonotic microbes. This study provides new insights into the cross-domain microbial ecology of hematophagous bats and underscores the need to integrate microbial community profiling with host behavioural data to enhance surveillance and mitigation strategies for zoonotic disease transmission.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s42523-025-00504-x.},
}
RevDate: 2026-02-22
CmpDate: 2026-02-20
Comparative analysis of rumen metagenomes with dietary supplementation of 3-nitrooxypropanol revealed divergent modes of action in hydrogen metabolism and reductant pathways between beef and dairy cattle.
Microbiome, 14(1):72.
BACKGROUND: The compound 3-nitrooxypropanol (3-NOP), an inhibitor of methyl-coenzyme M reductase (MCR), reduces enteric methane production in both beef and dairy cattle. Although the proposed mechanisms of 3-NOP involve on inhibiting the activity of MCR in vivo, it is unknown how this process could affect rumen microbiome as a whole and if it differs between beef and dairy cattle. This study conducted a comparative analysis of the rumen microbiome and its functional shifts in four different cattle studies (two beef and two dairy cattle studies) that evaluated 3-NOP supplementation using metataxonomics and metagenomics.
RESULTS: Comparative analysis of 281 rumen metataxonomic datasets (143 beef and 138 dairy cattle) revealed that dietary supplementation with 3-NOP affected rumen bacteria and methanogens. Further, comparative analysis of 54 metagenomic datasets (24 beef and 30 dairy cattle) revealed that 3-NOP inhibited mcrA, decreased the abundances of Methanobrevibacter gottschalkii and the protozoal species Isotricha prostoma, while increased the abundances of Methanobrevibacter ruminantium and Methanosphaera sp., Prevotella sp. was a significant bacterial taxon in both beef and dairy cattle, contributing to various pathways such as propionate and butyrate production. Its increased abundance after 3-NOP supplementation may also be linked to the decrease in Isotricha prostoma. Hydrogenotrophic methanogenesis decreased after 3-NOP supplementation with the abundance of genes involved in methylenetetrahydromethanopterin dehydrogenase decreased in beef cattle, while that of 4Fe-4S ferredoxin gene decreased in dairy cattle. The abundance of protozoal Polyplastron multivesiculatum increased after long-term 3-NOP supplementation in beef cattle, potentially due to changes in hydrogen (H2) partial pressure. During 3-NOP-mediated methanogenesis reduction, abundance of genes encoding methanogenic hydrogenase and H2 producing hydrogenase were decreased, while those encoding H2 sensory hydrogenase increased. Acyl-CoA dehydrogenase gene involved in propionate and butyrate production pathways increased in both beef and dairy cattle, while nitrite reductase increased specifically in beef cattle, indicating a rise in alternative H2 sinks. Video Abstract CONCLUSION: Our findings revealed broad effects of 3-NOP on rumen microbiome and functions in vivo, with varied effects in beef and dairy cattle, which provide mechanistic insights into the supplementation of 3-NOP in both beef and dairy cattle, supporting its more sustainable and effective use in the future.
Additional Links: PMID-41715233
PubMed:
Citation:
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hide bibtex listing
@article {pmid41715233,
year = {2026},
author = {Choi, Y and Zhou, M and Oba, M and Romero-Pérez, A and Beauchemin, KA and Duval, S and Kindermann, M and Guan, LL},
title = {Comparative analysis of rumen metagenomes with dietary supplementation of 3-nitrooxypropanol revealed divergent modes of action in hydrogen metabolism and reductant pathways between beef and dairy cattle.},
journal = {Microbiome},
volume = {14},
number = {1},
pages = {72},
pmid = {41715233},
issn = {2049-2618},
support = {Award ID 22-000373//Foundation for Food & Agriculture Research Greener Cattle Initiative/ ; Award ID 22-000373//Foundation for Food & Agriculture Research Greener Cattle Initiative/ ; Award ID 22-000373//Foundation for Food & Agriculture Research Greener Cattle Initiative/ ; FDE.18.21C//Beef Cattle Research Council Cluster/ ; FDE.18.21C//Beef Cattle Research Council Cluster/ ; ALLRP 588541-23//Natural Sciences and Engineering Research Council of Canada (NSERC) Discovery and NSERC Alliance program/ ; ALLRP 588541-23//Natural Sciences and Engineering Research Council of Canada (NSERC) Discovery and NSERC Alliance program/ ; },
mesh = {Metagenome ; *Rumen/enzymology/microbiology ; Animals ; *Cattle/microbiology ; Dietary Supplements ; *Gastrointestinal Microbiome/drug effects ; *Propanols/pharmacology ; Fatty Acids, Volatile/biosynthesis ; *Methane/biosynthesis ; Hydrogen/metabolism ; Metabolic Networks and Pathways/drug effects ; },
abstract = {BACKGROUND: The compound 3-nitrooxypropanol (3-NOP), an inhibitor of methyl-coenzyme M reductase (MCR), reduces enteric methane production in both beef and dairy cattle. Although the proposed mechanisms of 3-NOP involve on inhibiting the activity of MCR in vivo, it is unknown how this process could affect rumen microbiome as a whole and if it differs between beef and dairy cattle. This study conducted a comparative analysis of the rumen microbiome and its functional shifts in four different cattle studies (two beef and two dairy cattle studies) that evaluated 3-NOP supplementation using metataxonomics and metagenomics.
RESULTS: Comparative analysis of 281 rumen metataxonomic datasets (143 beef and 138 dairy cattle) revealed that dietary supplementation with 3-NOP affected rumen bacteria and methanogens. Further, comparative analysis of 54 metagenomic datasets (24 beef and 30 dairy cattle) revealed that 3-NOP inhibited mcrA, decreased the abundances of Methanobrevibacter gottschalkii and the protozoal species Isotricha prostoma, while increased the abundances of Methanobrevibacter ruminantium and Methanosphaera sp., Prevotella sp. was a significant bacterial taxon in both beef and dairy cattle, contributing to various pathways such as propionate and butyrate production. Its increased abundance after 3-NOP supplementation may also be linked to the decrease in Isotricha prostoma. Hydrogenotrophic methanogenesis decreased after 3-NOP supplementation with the abundance of genes involved in methylenetetrahydromethanopterin dehydrogenase decreased in beef cattle, while that of 4Fe-4S ferredoxin gene decreased in dairy cattle. The abundance of protozoal Polyplastron multivesiculatum increased after long-term 3-NOP supplementation in beef cattle, potentially due to changes in hydrogen (H2) partial pressure. During 3-NOP-mediated methanogenesis reduction, abundance of genes encoding methanogenic hydrogenase and H2 producing hydrogenase were decreased, while those encoding H2 sensory hydrogenase increased. Acyl-CoA dehydrogenase gene involved in propionate and butyrate production pathways increased in both beef and dairy cattle, while nitrite reductase increased specifically in beef cattle, indicating a rise in alternative H2 sinks. Video Abstract CONCLUSION: Our findings revealed broad effects of 3-NOP on rumen microbiome and functions in vivo, with varied effects in beef and dairy cattle, which provide mechanistic insights into the supplementation of 3-NOP in both beef and dairy cattle, supporting its more sustainable and effective use in the future.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Metagenome
*Rumen/enzymology/microbiology
Animals
*Cattle/microbiology
Dietary Supplements
*Gastrointestinal Microbiome/drug effects
*Propanols/pharmacology
Fatty Acids, Volatile/biosynthesis
*Methane/biosynthesis
Hydrogen/metabolism
Metabolic Networks and Pathways/drug effects
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ESP Quick Facts
ESP Origins
In the early 1990's, Robert Robbins was a faculty member at Johns Hopkins, where he directed the informatics core of GDB — the human gene-mapping database of the international human genome project. To share papers with colleagues around the world, he set up a small paper-sharing section on his personal web page. This small project evolved into The Electronic Scholarly Publishing Project.
ESP Support
In 1995, Robbins became the VP/IT of the Fred Hutchinson Cancer Research Center in Seattle, WA. Soon after arriving in Seattle, Robbins secured funding, through the ELSI component of the US Human Genome Project, to create the original ESP.ORG web site, with the formal goal of providing free, world-wide access to the literature of classical genetics.
ESP Rationale
Although the methods of molecular biology can seem almost magical to the uninitiated, the original techniques of classical genetics are readily appreciated by one and all: cross individuals that differ in some inherited trait, collect all of the progeny, score their attributes, and propose mechanisms to explain the patterns of inheritance observed.
ESP Goal
In reading the early works of classical genetics, one is drawn, almost inexorably, into ever more complex models, until molecular explanations begin to seem both necessary and natural. At that point, the tools for understanding genome research are at hand. Assisting readers reach this point was the original goal of The Electronic Scholarly Publishing Project.
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Usage of the site grew rapidly and has remained high. Faculty began to use the site for their assigned readings. Other on-line publishers, ranging from The New York Times to Nature referenced ESP materials in their own publications. Nobel laureates (e.g., Joshua Lederberg) regularly used the site and even wrote to suggest changes and improvements.
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When the site began, no journals were making their early content available in digital format. As a result, ESP was obliged to digitize classic literature before it could be made available. For many important papers — such as Mendel's original paper or the first genetic map — ESP had to produce entirely new typeset versions of the works, if they were to be available in a high-quality format.
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With the development of methods for adding typeset side notes to PDF files, the ESP project now plans to add annotated versions of some classical papers to its holdings. We also plan to add new reference and pedagogical material. We have already started providing regularly updated, comprehensive bibliographies to the ESP.ORG site.
ESP Picks from Around the Web (updated 28 JUL 2024 )
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Fossils of miniature humans (hobbits) discovered in Indonesia
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Dinosaur tail, complete with feathers, found preserved in amber.
Astronomy
Mysterious fast radio burst (FRB) detected in the distant universe.
Big Data & Informatics
Big Data: Buzzword or Big Deal?
Hacking the genome: Identifying anonymized human subjects using publicly available data.