Gut Microbes最新文献

{"title":"A novel exopolysaccharide from <i>Lactiplantibacillus plantarum</i> H6 improves cholesterol metabolism via <i>Muribaculum-</i>mediated activation of the enterohepatic FXR-FGF15 axis.","authors":"Yue Li, Jialin Wang, Hailing Wang, Xin Ma, Dayong Ren, Binghua Wang","doi":"10.1080/19490976.2026.2623578","DOIUrl":"10.1080/19490976.2026.2623578","url":null,"abstract":"<p><p>Hypercholesterolemia is a major risk factor for atherosclerotic cardiovascular disease; however, current therapeutic options such as statins are limited by issues including hepatotoxicity and patient intolerance. Probiotics and their metabolites show promise in modulating cholesterol metabolism through the gut‒liver axis, yet the specific commensal bacteria and molecular mechanisms underlying these effects remain poorly understood. In this study, we isolated and characterized EPS-D1, a novel exopolysaccharide (15.003 kDa) derived from <i>Lactiplantibacillus plantarum</i> H6, which is composed primarily of mannose (46.10%) and glucose (33.98%) and features a highly branched structure (branching degree of 29.5%). The administration of EPS-D1 significantly reduced the serum total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) by 40.31%, 37.55%, and 43.15%, respectively, in high-cholesterol diet (HCD) mice. Additionally, it improved hepatic steatosis and reduced markers of liver injury. Through 16S rRNA sequencing and fecal microbiota transplantation (FMT), we identified <i>Muribaculum</i> as the key commensal bacterium enriched by EPS-D1. Direct administration of <i>Muribaculum</i> (<i>Muribaculum intestinale</i>) replicated the cholesterol-lowering effects, decreasing ileal and fecal cholesterol levels by 74.79% and 53.16%, respectively. Mechanistically, both EPS-D1 and <i>M. intestinale</i> activated the enterohepatic FXR‒FGF15 axis, which resulted in the upregulation of hepatic cholesterol 7α-hydroxylase (CYP7A1) expression and the downregulation of ileal ASBT and NPC1L1, thereby promoting bile acid synthesis and inhibiting cholesterol absorption. Furthermore, <i>M. intestinale</i> increased intestinal short-chain fatty acids (SCFAs), particularly acetic acid and caproic acid, by 37.88% while also modulating the composition of the bile acid pool. These findings establish <i>M. intestinale</i> as a precise microbial target for cholesterol management and demonstrate that EPS-D1 from <i>L. plantarum</i> H6 enhances cholesterol metabolism through microbiota-mediated activation of the enterohepatic FXR‒FGF15 axis, providing a novel therapeutic strategy for managing hypercholesterolemia.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2623578"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146099619","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":"Intestinal epithelial Syndecan-1 maintains mucosal homeostasis in inflammatory bowel disease by enhancing <i>Faecalibacterium prausnitzii</i> biofilm formation.","authors":"Shuze Chen, Hanxiao Feng, Ying Wang, Jun Huang, Senbao Xu, Yunying Gong, Xiuying Liu, Ye Ouyang, Qiujuan Ye, Dekai Zheng, Kai Sun, Anjiang Wang, Ye Chen","doi":"10.1080/19490976.2026.2665870","DOIUrl":"10.1080/19490976.2026.2665870","url":null,"abstract":"<p><p>Despite the rising global incidence of inflammatory bowel disease (IBD), curative therapies remain unavailable. While our previous work implicated the intestinal proteoglycan Syndecan-1 (SDC1) in IBD-associated barrier dysfunction and inflammation, the underlying mechanism was unclear. This study aimed to elucidate how SDC1 maintains intestinal barrier integrity through interactions with the gut microbiome. In DSS-induced colitis, global knockout of <i>Sdc1</i> (<i>Sdc1</i>^<i>-/-</i>) exhibited exacerbated inflammatory infiltration and greater impairment of barrier structure and function than wild-type (WT). Formation of intestinal organoids was independent of genotype, indicating that <i>Sdc1</i>^<i>-/-</i> does not impair barrier function via disrupting epithelial development. The heightened colitis susceptibility in <i>Sdc1</i>^<i>-/-</i> mice was abolished in the antibiotic-treated pseudo-germ-free models, and transmissible to WT mice via fecal microbiota transplantation. Similar results were reproduced in a germ-free mouse model. Metagenomic sequencing identified <i>Faecalibacterium prausnitzii</i> as the most significantly depleted species upon <i>Sdc1</i> knockout. <i>In vitro</i>, SDC1-attached glycosaminoglycans (heparan sulfate (HS) and chondroitin sulfate (CS)) but not the SDC1 core protein promoted <i>F. prausnitzii</i> growth. Prokaryotic transcriptome profiling indicated that HS/CS induces cobalamin biosynthesis in <i>F. prausnitzii</i>. The critical role of cobalamin as a mediator was confirmed, as its synthetic inhibition significantly diminished the growth-promoting effect of HS/CS. Mechanism studies showed that HS/CS enhanced biofilm formation in <i>F. prausnitzii</i>, thereby facilitating cobalamin biosynthesis. Oral administration of HS ameliorated DSS-induced colitis and promoted mucosal colonization of <i>F. prausnitzii</i>, independent of the host genotype. Finally, human IBD biopsies revealed a positive correlation between epithelial SDC1 and mucosal <i>F. prausnitzii,</i> as well as an inverse correlation with bacterial translocation and the number of LPS‑positive cells. Our study elucidates a novel mechanism in which the glycosaminoglycan chains of SDC1 promote <i>F. prausnitzii</i> colonization and growth through enhanced biofilm formation and cobalamin synthesis, thereby highlighting the therapeutic potential of HS for IBD and offering a new basis for host-directed microbiota regulation.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2665870"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13138079/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147814511","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":"Early postnatal antibiotic-associated gut microbiota alterations might promote long-term lipid metabolism via brown adipose tissue metabolic programming.","authors":"Huijing Liang, Fengling Jiang, Lei Ren, Xiaoting Li, Simou Wu, Jinxing Li, Liang Li, Xiaolei Ze, Xi Shen, Fang He","doi":"10.1080/19490976.2026.2665885","DOIUrl":"https://doi.org/10.1080/19490976.2026.2665885","url":null,"abstract":"<p><p>The Developmental Origins of Health and Disease theory describes early life as a critical window for long-term metabolic health. Accumulating evidence has identified the gut microbiota as a key mediator of early-life metabolic programming. This study utilized antibiotic intervention in neonatal mice to investigate the long-term effects of early postnatal gut microbiota perturbations on adult lipid metabolism and examined the underlying mechanisms involving both thermogenic adipose tissue programming and microbiota structural remodeling. We found that early postnatal antibiotic exposure significantly disrupted the normal developmental assembly of the gut microbiota. Surprisingly, these alterations were associated with partial attenuation of high‑fat diet‑induced lipid metabolic disturbances in adulthood, an effect that was more pronounced in male mice than in female mice. Mechanistically, the observed metabolic improvement appeared to be associated with brown adipose tissue (BAT) thermogenic activation rather than with white adipose tissue browning or persistent gut microbiota restructuring. Early postnatal antibiotic exposure-associated gut microbiota alterations were linked to enhanced BAT development, potentially via interleukin-6 signaling and M2 macrophage polarization, suggestive of a metabolic programming effect that enhanced adaptive thermogenesis and improved long-term lipid homeostasis. These findings indicate that the gut microbiota might represent a modifiable factor influencing adipose tissue development, highlighting the potential of targeting the microbiota-BAT interplay in early life for obesity prevention strategies.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2665885"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837076","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":"A novel bile salt hydrolase-producing <i>Ligilactobacillus salivarius</i> prevents diet-induced obesity via regulation of bile acid metabolism and glucagon-like peptide 1 restoration.","authors":"Jiayao Lv, Lanqi Zhou, Xiaoshuang Dai, Rikard Landberg, Huicui Meng, Honglei Tian, Shiyi Zhang, Tianqi Liu, Xiaochen Yin, Jiayi Zhang, Xizi Song, Christophe Bonny, Stephanie Blum, Youshen Cao, Jingyao Guo, Wen Peng, Yan Tan, Lin Shi","doi":"10.1080/19490976.2026.2668127","DOIUrl":"https://doi.org/10.1080/19490976.2026.2668127","url":null,"abstract":"<p><p>Obesity poses a major global health challenge, necessitating safe and effective therapeutic strategies. Using high-throughput genomic screening for bile salt hydrolase (BSH)-producing strains, we identified <i>Ligilactobacillus salivarius</i> (<i>L. salivarius</i>) XA1416, a strain isolated from the feces of healthy individuals, which exhibits high BSH activity, strong acid resistance, and efficient colonization in the gastrointestinal tract. Oral administration of <i>L. salivarius</i> XA1416 counteracted high-fat diet-induced weight gain in mice, improved glucose homeostasis, and enhanced GLP-1 secretion. The strain modulated the gut microbiota, enriching taxa such as <i>Bacteroides</i>, <i>Alistipes</i>, and <i>Faecalibaculum</i>, and altered bile acid profiles, notably increasing ursodeoxycholic acid (UDCA). Mendelian randomization analysis leveraging large-scale human GWAS data and two cross-sectional cohorts' data, complemented by <i>in vitro</i> fecal microbiota fermentation experiments, collectively supports a key role of UDCA in weight control. The oral administration of UDCA recapitulated the anti-obesity effects and metabolic benefits of XA1416, functioning as an intestinal Farnesoid X receptor antagonist and Takeda G-protein-coupled receptor 5 agonist to stimulate GLP-1 secretion. This mechanism likely involves modulation of the hepatic FXR/SHP/SREBP-1c pathway and concurrent activation of the GLP-1 receptor, contributing to improved metabolic homeostasis. Additionally, we gavaged the mice fed with normal chow or a high-fat diet with GR-7, a specific inhibitor of microbial BSHs, leading to a reduction in UDCA level and GLP-1 production. Using HepG2 cell models and molecular dynamics simulations, we further demonstrated that UDCA directly activates the GLP-1 receptor. Taken together, our findings position <i>L. salivarius</i> XA1416 as a promising anti-obesity probiotic, with UDCA serving as a key microbial metabolite that mediates its beneficial metabolic effects.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2668127"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837090","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":"<b>Peptidoglycan from</b> <i><b>Bifidobacterium adolescentis</b></i> <b>enhances IL-10 production in regulatory B cells to alleviate gut inflammation</b>.","authors":"Sohyeon Lee, Yoonho Lee, Ho-Su Lee, Jiyoung Yu, Kyunggon Kim, Tae-Young Kim, Su-Hyun Lee, Yuan Qiao, Seungil Kim, Mi-Na Kweon","doi":"10.1080/19490976.2025.2611603","DOIUrl":"10.1080/19490976.2025.2611603","url":null,"abstract":"<p><p>The mechanisms by which gut microbiota modulate host immune responses remain incompletely understood. Here, we screened <i>Lactobacillus</i> and <i>Bifidobacterium</i> strains isolated from healthy individuals to identify symbionts capable of suppressing gut inflammation. Among them, <i>Bifidobacterium adolescentis</i> (Bifi-94) induced IL-10 production in mononuclear cells <i>in vitro</i>. Oral administration of Bifi-94 to mice treated with dextran sulfate sodium attenuated weight loss and reduced colonic inflammation scores. In wild-type C57BL/6 mice, Bifi-94 increased IL-10 levels in colonic tissue homogenates without altering the frequency of regulatory T cells. Instead, CD19⁺CD11b⁺ regulatory B (Breg) cells emerged as the primary source of IL-10, with their numbers significantly increasing in the peritoneal cavity (PEC) after treatment. IL-10 secretion by PEC cells was robustly activated by live, heat-killed, and formalin-fixed Bifi-94. Bifi-94-derived peptidoglycan (PG) selectively stimulated IL-10 production in CD19⁺CD11b⁺ Breg cells, and multi-omics analyses showed that Bifi-94 exhibits increased expression of PG biosynthetic enzymes (MurE, MurD, Alr, UppP) relative to the type strain. Mechanistically, Bifi-94-derived PG promoted TLR2-dependent activation of ERK and p38 MAPK signaling in Breg cells. Notably, PG similarly enhanced IL-10 production in CD19⁺ B cells from human colonic tissue. These findings demonstrate that Bifi-94-derived PG promotes IL-10 production in Breg cells via TLR2-mediated signaling, thereby contributing to the attenuation of gut inflammation.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2611603"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12795277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145933099","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-lung axis and microbiome alterations in mycobacterial infections: from pathogenesis to therapeutic potential.","authors":"Kimin Kang, Joong-Yub Kim, Jae-Joon Yim, Donghyun Kim","doi":"10.1080/19490976.2025.2612428","DOIUrl":"10.1080/19490976.2025.2612428","url":null,"abstract":"<p><p>Mycobacterial lung diseases, including tuberculosis (TB) and nontuberculous mycobacterial pulmonary disease (NTM-PD), are increasingly recognized as disorders influenced not only by host immunity but also by microbiota. Emerging evidence identifies the gut-lung axis (GLA) as a key bidirectional communication network linking intestinal and pulmonary homeostasis. Mycobacterial infection itself induces airway and gut dysbiosis through immune and metabolic disturbances, which is further exacerbated by prolonged antibiotic therapy. Dysbiosis within either site reciprocally affects the other via GLA, leading to reduced microbial diversity, impaired epithelial integrity, and systemic inflammation. These alterations disrupt metabolite-mediated immunoregulation and attenuate IL-22-driven epithelial defense, thereby weakening bacterial clearance and promoting chronic inflammation. Distinct microbial features, such as the depletion of beneficial SCFA-producing taxa and enrichment of pro-inflammatory anaerobes, are observed in both TB and NTM-PD. Moreover, therapy-induced microbiome remodeling influences treatment response and disease relapse. Restoring microbial balance through probiotics, prebiotics, postbiotics, dietary modulation, or fecal microbiota transplantation offers a promising adjunctive strategy. This review integrates current evidence linking microbiome dysbiosis to mycobacterial pathogenesis and highlights microbiome-targeted interventions as an emerging therapeutic frontier in pulmonary mycobacterial diseases.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2612428"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12785239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145917505","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 microbiome-derived propionate reprograms alveolar macrophages metabolically and regulates lung injury responses in mice.","authors":"Daisuke Maruyama, Xiaoli Tian, Thien N M Doan, Wen-I Liao, Tomohiro Chaki, Hiroki Taenaka, Mazharul Maishan, Michael A Matthay, Arun Prakash","doi":"10.1080/19490976.2025.2606486","DOIUrl":"10.1080/19490976.2025.2606486","url":null,"abstract":"<p><p>Responses to lung injury can vary between individuals with the diet and gut microbiome representing two underappreciated sources for this variability. The gut microbiome can influence lung injury outcomes through the gut‒lung axis, but exactly how diet and its effects on the microbiota are involved remains unclear. We hypothesized that dietary fiber interventions would favor the presence of short-chain fatty acid (SCFA)-producing fermentative bacteria presence in the gut microbiome, thereby influencing the resting lung immunometabolic tone as well as influencing downstream responses to lung injury and infection. To test this hypothesis, we fed mice fiber-rich (FR) and fiber-free (FF) diets, and observed changes in the steady-state transcriptional programming of alveolar macrophages (AM). Next, we examined the effects of the FR and FF diets on murine responses to sterile and infectious lung injury <i>in vivo</i> while simultaneously profiling the gut microbiota and SCFA levels transmitted along the gut‒lung axis. Finally, we validated our <i>in vivo</i> observations with mechanistic studies of the metabolic, signaling, and chromatin-modifying effects of specific SCFAs on lung AM <i>ex vivo</i> and <i>in vitro</i>. Overall, our fiber-rich diet reprogrammed AMs and attenuated lung inflammation after sterile injury while exacerbating lung infection. This effect of FR diets could be transferred to germ-free (GF) mice by fecal microbiome transplantation (FMT) and depended on the ability of the microbiota to produce propionate. Mechanistically, SCFAs altered the metabolic programming of AMs and lung tissue <i>ex vivo</i> without a clear role for free fatty acid receptors (FFAR) or chromatin remodeling. These findings demonstrate that the gut‒lung axis can regulate resting lung metabolic tone through dietary fiber intake and the enrichment of SCFA-producing gut bacteria, as well as influence sterile and non-sterile lung injury responses. These results provide evidence to support the development of therapeutic dietary interventions to preserve or enhance specific aspects of host pulmonary immunity.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2606486"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12758369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145855473","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 and immunometabolism in obesity.","authors":"Alba Torres-Mayo, Rebeca Liébana-García, Marta Olivares, Aize Pellón, Juan Anguita, Yolanda Sanz","doi":"10.1080/19490976.2026.2667610","DOIUrl":"https://doi.org/10.1080/19490976.2026.2667610","url":null,"abstract":"<p><p>The gut microbiota plays a central role in modulating both immunity and metabolism. Obesity-associated microbiota configuration is a critical driver of persistent inflammatory activation and immune dysfunction, ultimately leading to chronic metabolic disorders. Immunometabolism examines how metabolic demands shape immune cell function and how immune responses influence cellular metabolism. Emerging research on how the gut microbiota contribute to immune cell metabolic processes and the resulting health outcomes is deepening our understanding of the mechanisms underlying obesity and metabolic diseases. In this review, we summarize how intracellular metabolic pathways and master regulators, such as mTOR and AMPK, orchestrate immune cell function and how their dysregulation contributes to obesity-associated immune and metabolic dysfunction. We also discuss how gut microbiota influences the immunometabolism of different myeloid and lymphoid cell subsets and intestinal epithelial cells. Finally, we review the role of microbially produced metabolites, including short-chain fatty acids, lactate, succinate, bile acids, and amino acids, in reprogramming immune cell metabolism. We also discuss whether modulating gut microbiota function to regulate immunometabolic pathways could help restore immune homeostasis and reduce obesity-related complications.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2667610"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837176","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":"The role of gut microbiota in chronic intestinal pseudo-obstruction: exploring fecal microbiota transplantation as a treatment option.","authors":"Giada De Palma, Anna Costanzini, Vidhyalakshmi Mohan, Sacha Sidani, Zarwa Saqib, Marc Pigrau, Jun Lu, Natalia Causada Calo, Ines Pinto-Sanchez, Elena F Verdu, Margaret Marcon, Giovanni Barbara, Vincenzo Stanghellini, Roberto De Giorgio, Stephen M Collins, Premysl Bercik","doi":"10.1080/19490976.2025.2610597","DOIUrl":"10.1080/19490976.2025.2610597","url":null,"abstract":"<p><p>Chronic intestinal pseudo-obstruction (CIPO) is characterized by bowel dilation and obstructive symptoms without any structural blockage. Although the microbiota is known to affect gastrointestinal function, its role in CIPO is poorly understood. We aimed to characterize the CIPO microbiota, investigate its role in disease expression and explore the therapeutic role of fecal microbiota transplantation (FMT). CIPO patients (<i>n</i> = 14) and healthy controls (HC, <i>n</i> = 12) were recruited from Italy and Canada. Microbiota profiles and functions were assessed by 16S rRNA sequencing and PICRUSt. Germ-free NIH Swiss mice were colonized with HC and CIPO microbiota, their intestinal transit and bowel distension were assessed by videofluoroscopy and computed tomography (CT), and the expression of host genes by NanoString®. The CIPO microbiota exhibited reduced microbial diversity with dominance of Proteobacteria and altered metabolic function. Mice with CIPO microbiota developed marked bowel distension and slow intestinal transit associated with altered expression of multiple genes related to immunity, the intestinal barrier and neuromuscular function. FMT from a HC improved the microbiota profile, intestinal transit and bowel distension in both CIPO mice and a selected CIPO patient, in whom a marked clinical improvement was sustained for 8 y. Thus, our findings support the use of microbiota-directed therapies to induce clinical improvement in CIPO patients.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"18 1","pages":"2610597"},"PeriodicalIF":11.0,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12785189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145917483","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":"https://doi.org/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":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}