Gut Microbes最新文献

{"title":"<i>Saccharomyces boulardii</i> CNCM I-745 synergizes with the small intestinal microbiota to boost AhR signaling in celiac disease.","authors":"Kelly R Kan, Marco Constante, Sara Rahmani, Gaston H Rueda, Mark Wulczynski, Maria Ines Pinto-Sanchez, Xavier Roux, Premysl Bercik, Heather J Galipeau, Alberto Caminero, Elena F Verdu","doi":"10.1080/19490976.2026.2664640","DOIUrl":"10.1080/19490976.2026.2664640","url":null,"abstract":"<p><p>Celiac disease (CeD) is an immune-mediated condition that leads to small intestinal villous atrophy and is driven by dietary gluten in individuals carrying HLA-DQ2 and DQ8. Microbial factors have been implicated in both the onset of CeD and persistent symptoms (non-responsive CeD) after the gluten-free diet (GFD), through mechanisms including impaired tryptophan metabolism and aryl hydrocarbon receptor (AhR) pathway activation. Although probiotics have been shown to be safe in CeD, there are currently no clinical recommendations for strains that target disease-related mechanisms. We here demonstrate that <i>S. boulardii</i> activated the AhR pathway in gluten-sensitized mice expressing HLA-DQ8, improving gluten-immunopathology. Mechanistically, <i>S. boulardii</i> enhanced the CeD patients' microbiota capacity for AhR activation when duodenal indole-producing commensals, such as <i>Lactobacillus reuteri</i>, were present. Our study provides preclinical evidence that <i>S. boulardii</i> CNCM I-745 targets a microbial deficiency previously described in CeD through modulation of microbial tryptophan metabolism. The findings encourage clinical testing of <i>S. boulardii</i> in CeD to prevent or better treat non-responsive cases.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2664640"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13138080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147814487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction.","authors":"","doi":"10.1080/19490976.2026.2667667","DOIUrl":"10.1080/19490976.2026.2667667","url":null,"abstract":"","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2667667"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13154955/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i><b>Akkermansia muciniphila</b></i> <b>modulates intestinal mucus composition to counteract high-fat diet-induced obesity in mice</b>.","authors":"Paola Paone, Camille Petitfils, Anthony Puel, Dimitris Latousakis, Willem M de Vos, Nathalie M Delzenne, Nathalie Juge, Matthias Van Hul, Patrice D Cani","doi":"10.1080/19490976.2025.2612580","DOIUrl":"10.1080/19490976.2025.2612580","url":null,"abstract":"<p><strong>Objective: </strong>This study investigates whether live <i>Akkermansia muciniphila</i> Muc^T supplementation can counteract obesity and metabolic dysfunctions induced by a high-fat diet (HFD) by modulating intestinal mucus production, secretion and composition.</p><p><strong>Design: </strong>C57BL/6J mice were fed an HFD with or without live <i>A. muciniphila</i> Muc^T (2 × 10⁸ CFU per day) supplementation or a control diet for 6 weeks. Body weight, fat mass gain and metabolic markers were measured. Intestinal mucus characteristics were assessed via gene expression analysis of mucins and analysed mucin glycosylation by tandem mass spectrometry (MS/MS).</p><p><strong>Results: </strong>Mice receiving live <i>A. muciniphila</i> Muc^T exhibited reduced body weight gain and fat mass accumulation compared to HFD controls, without changes in muscle mass. <i>A. muciniphila</i> improved gut barrier integrity by increasing antimicrobial peptide expression in the jejunum and in the colon of HFD-fed mice. Furthermore, live <i>A. muciniphila</i> Muc^T influenced markers of goblet cell differentiation and restored the expression of mucin markers altered by HFD. Specifically, live <i>A. muciniphila</i> Muc^T counteracted HFD-induced mucin 3 (Muc3) expression depletion in the colon. Although the overall mucus thickness was not affected by live <i>A. muciniphila</i> Muc^T, the bacteria significantly modulated mucin glycans composition. Live <i>A. muciniphila</i> Muc^T did not change the gut microbiota composition.</p><p><strong>Conclusion: </strong>These findings highlight the protective effects of live <i>A. muciniphila</i> Muc^T against diet-induced metabolic dysfunctions by modulating adiposity, mucus layer composition, and glycan profiles. This reinforces its potential as a therapeutic strategy for metabolic disorders associated with gut microbiota alterations.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2612580"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12795273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145933125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GutMIND: A multi-cohort machine learning framework for integrative characteristics of the microbiota-gut-brain axis in neuropsychiatric disorders.","authors":"Yanmei Ju, Shutian Lin, Shaohua Hu, Xin Jin, Liang Xiao, Tao Zhang, Yudan Zhang, Liping Zhang, Xiancang Ma, Feng Zhu, Ruijin Guo","doi":"10.1080/19490976.2026.2630563","DOIUrl":"10.1080/19490976.2026.2630563","url":null,"abstract":"<p><p>Emerging evidence underscores bidirectional communication along the microbiota-gut-brain axis in neuropsychiatric disorders. However, the field lacks dedicated metagenomic resources with standardized phenotyping for these conditions. Existing single-cohort studies face inherent limitations due to restricted sample sizes, confounding heterogeneity, and methodological fragmentation, compromising reproducibility and mechanistic insights. To overcome these challenges, we constructed the Gut Microbiome in Multinational Integrated Neuropsychiatric Disorders (GutMIND) database, a comprehensive resource integrating shotgun metagenomic data with harmonized metadata. Adhering to a standardized preprocessing protocol and rigorous quality control workflow, this dataset represents the largest gut-brain microbiome repository to date, encompassing 31 studies across 12 countries (<i>n</i> = 3,492) spanning 14 neuropsychiatric conditions. Utilizing this dataset, we characterized microbial community heterogeneity, which was significantly elevated in patients compared to healthy controls. Subsequently, we developed a computational framework, MetaClassifier, enabling the diagnosis of neuropsychiatric disorders and the identification of microbial biomarkers. Employing a comprehensive two-stage validation strategy, we first assessed the model utilizing taxonomic abundance profiles via nested cross-validation in the high-quality discovery cohort (<i>n</i> = 2,734), achieving a mean AUROC of 0.69 (range: 0.55-0.78) across 8 disorders. Its robustness was further confirmed in an independent platform-extended validation cohort (<i>n</i> = 400), yielding a mean AUROC of 0.71 (range: 0.60-0.76). We also developed the Microbial Gut-Brain Axis Health Index (MGBA-HI), which effectively distinguished neuropsychiatric status in both the high-quality cohort and the platform-extended cohort. Furthermore, integrative analysis of health-abundant species, index-derived biomarkers, and ecological prevalence, we identified 9 core neuropsychiatric-protective microbiota. These species predominantly exhibited metabolic capacities linked to glutamate synthesis and acetate production. Building upon this, the GutMIND framework ensures robust cross-cohort comparability while minimizing technical heterogeneity, thereby enhancing inferential rigor in gut microbiome-neuropsychiatry research. Notably, the MetaClassifier, MGBA-HI, and core microbiota hold translational potential for developing microbiome-based prognostic tools and personalized therapeutic strategies in neuropsychiatric disorders. The source code and usage instructions for MetaClassifier are accessible at https://github.com/juyanmei/MetaClassifier.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2630563"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146201408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular vesicles and their RNA cargo facilitate bidirectional cross-kingdom communication between human and bacterial cells.","authors":"Laura Gröger, Shusruto Rishik, Nicole Ludwig, Amila Beganovic, Marcus Koch, Stefanie Rheinheimer, Martin Hart, Petra König, Tabea Trampert, Pascal Paul, Annette Boese, Claus-Michael Lehr, Sören L Becker, Gregor Fuhrmann, Andreas Keller, Eckart Meese","doi":"10.1080/19490976.2026.2630482","DOIUrl":"10.1080/19490976.2026.2630482","url":null,"abstract":"<p><p>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 <i>Lacticaseibacillus casei</i>, <i>Enterococcus faecalis</i>, and <i>Proteus mirabilis</i> induce distinct transcriptomic changes in Caco-2 cells depending on the bacterial species, with up to ~6,000 differentially expressed genes, including <i>CCL20</i>, <i>CXCL8</i>, or <i>CXCL10</i>. 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.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2630482"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12928640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146258046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Clostridium butyricum</i> alleviates multiple myeloma by remodeling the bone marrow microenvironment and inhibiting PI3K/AKT pathway through the gut‒bone axis.","authors":"Jingyu Wang, Fuming Zi, Wu Liu, Chengrui Liu, Zhengfeng Zhang, Leilei Kong, Xuan Xu, Jing Wei, Tingtao Chen, Jian Li","doi":"10.1080/19490976.2025.2609455","DOIUrl":"10.1080/19490976.2025.2609455","url":null,"abstract":"<p><p>Emerging evidence reveals a strong connection between the gut microbiota and cancer. However, the exact role of gut microbiota dysbiosis in multiple myeloma (MM) is poorly understood, and the therapeutic potential of microbiota-targeted interventions represents a promising strategy that demands urgent mechanistic and translational investigation. First, we conducted a comprehensive microbiome-metabolite analysis between MM patients and healthy individuals. The result revealed a marked compositional difference characterized by reduced abundances of butyrate-producing bacteria and diminished butyrate levels in the MM cohort. Subsequent fecal microbiota transplantation demonstrated that the gut microbiota critically modulates MM progression, with healthy donor-derived microbiota reducing the tumor burden and concomitantly elevating serum butyrate. Furthermore, through function-based culturomics screening, <i>Clostridium butyricum</i> (<i>C. butyricum</i>) was identified as a key butyrate-producing specialist. <i>C. butyricum</i> or its metabolite butyrate significantly reduced the systemic tumor burden in 5TGM1 mice. Notably, <i>C. butyricum</i> and butyrate alleviated bone marrow inflammation and osteolytic lesions by suppressing Th17 cells and IL-17 levels in the bone marrow. Moreover, cellular assays and transcriptome sequencing further revealed that butyrate could induce MM cells' apoptosis via HDAC inhibition-mediated upregulation of PPARγ, leading to sequential suppression of the PI3K/AKT pathway and antiapoptotic BCL-2 expression. This apoptotic signaling cascade was reversed by PPARγ antagonism. The direct antitumor effect was further confirmed in M-NSG mice. Our research systematically verifies the specific role of the gut microbiota in MM and provides the first evidence of the immune and molecular mechanisms by which <i>C. butyricum</i> alleviates MM progression, offering preclinical support for probiotic-based therapies against MM.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2609455"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12773645/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145892365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut microbiota-associated nutritional-immune status predicts prognosis in postoperative NSCLC patients.","authors":"Qian Yu, Anqi Chen, Junqi Yi, Majid Iqbal, Ziying Tang, Huabo Ge, Yan Hu, Wenliang Liu, Leliang Zheng, Jingqun Tang, Juanjuan Xiang","doi":"10.1080/19490976.2026.2652460","DOIUrl":"10.1080/19490976.2026.2652460","url":null,"abstract":"<p><strong>Background: </strong>Surgical resection is the primary treatment for non-small cell lung cancer (NSCLC) patients with stages I and II; however, the postoperative prognosis varies among individuals. The prognostic nutritional index (PNI) reflects the nutritional-immune status of patients, but its microbial determinants remain unclear.</p><p><strong>Methods: </strong>PNI was analyzed in a cohort of 372 retrospective and 139 prospective NSCLC patients. This analysis integrated gut microbiota signatures using 16S rRNA sequencing, fecal metabolomics, and murine fecal microbiota transplantation (FMT) models.</p><p><strong>Results: </strong>A PNI value of ≥46.2 stratified postoperative NSCLC patients with improved 5-y survival (HR = 0.3889, 95% CI 0.2840-0.5356, <i>p</i> < 0.001). Patients with a high PNI showed enrichment of short-chain fatty acid (SCFA)-producing taxa, such as <i>Akkermansia</i> and <i>Eubacterium hallii</i>, and elevated butyrate/isovalerate levels, correlating with increased infiltration of CD8⁺ T cells (Pearson <i>r</i> = 0.51, <i>p</i> = 0.02). FMT from high-PNI patients reduced lung tumor growth in mice compared with FMT from low-PNI patients (7.2 vs 18 nodules, <i>p</i> = 0.01). Oral administration of <i>A. muciniphila</i> or/and <i>E. hallii</i> or butyrate suppressed tumor growth and enhanced CD8⁺ tumor-infiltrating lymphocytes (TILs) (<i>p</i> < 0.001).</p><p><strong>Conclusion: </strong>PNI and its linked gut microbiota‒SCFA axis are clinically prognostic biomarkers and potential immunomodulatory targets for early-stage NSCLC. Targeting this axis may serve as a promising coadjuvant strategy for NSCLC patients undergoing surgical resection.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2652460"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147616227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut microbiota-regulated glutathione metabolic rhythms restore obesity-induced colonic inflammatory oscillations.","authors":"Zhenting Zhao, Renjie Shi, Jin Ye, Danna Wang, Beita Zhao, Bo Ren, Luanfeng Wang, Xiaoning Liu, Xuebo Liu","doi":"10.1080/19490976.2026.2670048","DOIUrl":"https://doi.org/10.1080/19490976.2026.2670048","url":null,"abstract":"<p><p>Obesity disrupts circadian inflammatory rhythms, a defining feature of metabolic syndrome. However, the mechanisms connecting microbial and host circadian communication remain unclear. By using the fermentable fiber fructo-oligosaccharide (FOS) to restore microbial rhythmicity, we found that a high-fat diet (HFD) disrupts microbiota-regulated oscillations in glutathione metabolism, thereby dampening colonic inflammatory rhythms independently of the core clock machinery. Fecal microbiota transplantation (FMT) further supported a causal role for rhythmic fecal microbial signals in restoring inflammatory oscillations. Integrated multi-omics analysis highlighted circadian glutathione metabolism as a prominent candidate pathway linking microbial rhythmicity to host inflammatory oscillations. Importantly, colon-specific knockdown of <i>Gclc</i>, the rate-limiting enzyme in glutathione synthesis, abolished the restorative effects of microbial rhythms, functionally positioning host glutathione metabolism as a critical downstream mediator. Collectively, our study supports the existence of a microbiota-glutathione axis that contributes to the regulation of colonic inflammatory rhythms, uncovering a new chronobiological layer of microbial control over host inflammation.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2670048"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147863949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temporal dynamics of gut biosynthetic gene clusters link persistent colonization and engraftment in fecal microbiota transplantation.","authors":"Fernando Garcia-Guevara, Tom Resink, Frederick Clasen, Mathias Uhlén, Adnane Achour, Saeed Shoaie","doi":"10.1080/19490976.2026.2634469","DOIUrl":"10.1080/19490976.2026.2634469","url":null,"abstract":"<p><p>The human gut microbiome carries a large array of biosynthetic gene clusters (BGCs) that encode the production of secondary metabolites, yet their temporal dynamics and role during microbial colonization remain largely unexplored. Here, we tracked BGCs profile over time in a cohort of healthy adults, and identified two distinct groups: persistent, which are stable over time, and transient, which are more sporadic. Functional annotations indicated persistent gene clusters are enriched in antibiotic resistance mechanisms, while transient ones more frequently carry virulence-associated genes. We then examined colonization of these two groups in the context of fecal microbiome transplantation. Our results show that persistent gene clusters exhibit higher colonization rates than transient ones. These findings contribute to our understanding of how microbial metabolites influence host health, potentially guiding future therapeutic strategies targeting the microbiome.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2634469"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12940132/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147305104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatial mapping of human colonic niches reveals rapid, mucus-specific microbiota disruption after bowel cleansing.","authors":"Bahtiyar Yilmaz, Sarah Moulin, Benjamin Heimgartner, Hai Li, Markus Geuking, Pascal Juillerat, Benjamin Misselwitz, Andrew J Macpherson, Reiner Wiest","doi":"10.1080/19490976.2026.2635866","DOIUrl":"10.1080/19490976.2026.2635866","url":null,"abstract":"<p><p>Bowel preparation is routinely performed before colonoscopy, yet its immediate effects on the spatial organization of the colonic microbiota at the mucosal interface remain poorly resolved. Here, we introduce a high-resolution endoscopic mucus-harvesting approach, combined with luminal aspirates and mucosal biopsies, to generate a high-resolution, within-subject trajectory of microbiota alterations across distinct colonic niches in healthy adults over the first 24 hours after purging. While luminal bacterial communities remained remarkably stable, with no significant changes in alpha or beta diversity and proportional washout of taxa. In contrast, mucus-associated and mucosal communities underwent a rapid but reversible ecological restructuring, characterized by immediate post-cleansing shifts in composition and transient blooms of Proteobacteria, particularly <i>Enterobacteriaceae</i>. These perturbations were strongest in the 0-12-hour window and varied by individual, consistent with the dominance of personalized baseline microbial signatures. Critically, spatially resolved sampling revealed a key refinement: the <i>Enterobacteriaceae</i> expansion was confined almost exclusively to the superficial mucus layer, a glycan-rich, dynamically oxygenated compartment that is particularly susceptible to mechanical disturbance during lavage, whereas deeper mucus and mucosa-associated communities remained comparatively stable. By 24 hours, both mucosal and mucus-associated microbiota had largely returned to their individualized pre-cleansing configurations, indicating rapid ecosystem resilience and suggesting that the deeper mucus layer functions as a protected microbial reservoir that reseeds the epithelium and lumen once normal physiology is restored. This compartment-specific recovery trajectory contrasts with the prolonged dysbiosis typically observed after antibiotics or infection, underscoring the need for spatially precise sampling to interpret microbiome data collected during clinical endoscopy. Together, these findings establish an endoscopic strategy for probing microbe-mucus interactions in humans and provide a conceptual and methodological framework for interpreting microbiome data obtained during clinical endoscopy.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2635866"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12940144/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147305115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}