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Involvement of toll-like receptor 5 in mouse model of colonic hypersensitivity induced by neonatal maternal separation

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World Journal of Gastroenterology 2022年第29期28卷 3903-3916页

作者： Geoffroy Mallaret Amandine Lashermes Mathieu Meleine Ludivine Boudieu Julie Barbier Youssef Aissouni Agathe Gelot benoit chassaing Andrew T Gewirtz Denis Ardid Frederic Antonio Carvalho Department of Pharmacology UMR 1107 NeuroDolUniversity of Clermont AuvergneClermont-Ferrand 63000France Department of Microbiology UniversitéParis-SaclayNational Research Institute for AgricultureFood and the EnvironmentAgroParisTechMicalis InstituteJouy-en-Josas 78350France Team“Mucosal Microbiota in Chronic Inflammatory Diseases” INSERM U1016CNRS UMR 8104UniversitéParis CitéParis 75014France Center for Inflammation Institute for Biomedical SciencesGeorgia State UniversityAtlantaGA30033United States Department of Pharmacology INSERM 1107 NeuroDOL/University of Clermont AuvergneClermont-Ferrand 63000France

BACKGROUND Chronic abdominal pain is the most common cause for gastroenterology consultation and is frequently associated with functional gastrointestinal disorders including irritable bowel syndrome and inflammatory bowel disease. These disorders present similar brain/gut/microbiota trialogue alterations, associated with abnormal intestinal permeability, intestinal dysbiosis and colonic hypersensitivity(CHS). Intestinal dysbiosis can alter colon homeostasis leading to abnormal activation of the innate immunity that promotes CHS, perhaps involving the toll-like receptors(TLRs), which play a central role in innate *** To understand the mechanisms between early life event paradigm on intestinal permeability, fecal microbiota composition and CHS development in mice with TLRs expression in *** Maternal separation model(NMS) CHS model, which mimics deleterious events in childhood that can induce a wide range of chronic disorders during adulthood were used. Colonic sensitivity of NMS mice was evaluated by colorectal distension(CRD) coupled with intracolonic pressure variation(IPV) measurement. Fecal microbiota composition was analyzed by 16S rRNA sequencing from weaning to CRD periods. TLR mRNA expression was evaluated in ***, the effect of acute intrarectal instillation of the TLR5 agonist flagellin(FliC) on CHS in adult naive wildtype mice was *** Around 50% of NMS mice exhibited increased intestinal permeability and CHS associated with intestinal dysbiosis, characterized by a significant decrease of species richness, an alteration of the core fecal microbiota and a specific increased relative abundance of flagellated bacteria. Only TLR5mRNA expression was increased in colonocytes of NMS mice with CHS. Acute intrarectal instillation of FliC induced transient increase of IPV, reflecting transient CHS *** Altogether, these data suggest a pathophysiological continuum between intestinal dysbiosis a

关键词： Chronic abdominal pain Colonic hypersensitivity Toll-like receptors Intestinal microbiota Early life events

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Tryptophan:A gut microbiota-derived metabolites regulating inflammation

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World Journal of Gastrointestinal Pharmacology and Therapeutics 2017年第1期8卷 7-9页

作者： Lucie Etienne-Mesmin benoit chassaing Andrew T Gewirtz Center for Inflammation Immunityand InfectionInstitute for Biomedical SciencesGeorgia State UniversityAtlantaGA 30303United States

Inflammatory bowel diseases(IBD), which comprise Crohn's disease and ulcerative colitis, are chronic intestinal disorders with an increased prevalence and incidence over the last decade in many different regions over the world. The etiology of IBD is still not well defined, but evidence suggest that it results from per-turbation of the homeostasis between the intestinal microbiota and the mucosal immune system, with the involvement of both genetic and environmental factors. Genome wide association studies, which involve large-scale genome-wide screening of potential polymorphism, have identified several mutations associated with IBD. Among them, Card9, a gene encoding an adapter molecule involved in innate immune response to fungi(via type C-lectin sensing) through the activation of IL-22 signaling pathway, has been identified as one IBD susceptible genes. Dietary compounds, which represent a source of energy and metabolites for gut bacteria, are also appreciated to be important actors in the etiology of IBD, for example by altering gut microbiota composition and by regulating the generation of short chain fatty acids. A noteworthy study published in the June 2016 issue of Nature Medicine by Lamas and colleagues investigates the interaction between Card9 and the gut microbiota in the generation of the microbiota-derived tryptophan metabolite. This study highlights the role of tryptophan in dampening intestinal inflammation in susceptible hosts.

关键词：肠的发炎色氨酸 Microbiota

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