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| 1 | Tryptophan:A gut microbiota-derived metabolites regulating inflammation显示文摘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. | Lucie Etienne-Mesmin Benoit Chassaing Andrew T Gewirtz | 2017 | World Journal of Gastrointestinal Pharmacology and Therapeutics2017，8，1： | 7 |
| 2 | The Commensal Microbiota and Enteropathogens in the Pathogenesis of Inflammatory Bowel Diseases显示文摘 | Benoit Chassaing Arlette Darfeuille–Michaud | 2011 | Gastroenterology2011，，6： | 6 |
| 3 | Crohn disease-associated adherent-invasive E. coli bacteria target mouse and human Peyer’s patches via long polar fimbriae显示文摘 | Chassaing Benoit Rolhion Nathalie de Vallée Amélie Salim Sa’ad Y Prorok-Hamon Maelle Neut Christel Campbell Batty J S?derholm Johan D Hugot Jean-Pierre Colombel Jean-Frédéric Darfeuille-Michaud Arlette | 2011 | Journal of Clinical Investigation2011，，3： | 1 |
| 4 | Involvement of toll-like receptor 5 in mouse model of colonic hypersensitivity induced by neonatal maternal separation显示文摘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 immunity.AIM To understand the mechanisms between early life event paradigm on intestinal permeability, fecal microbiota composition and CHS development in mice with TLRs expression in colonocytes.METHODS 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 colonocytes.Additionally, the effect of acute intrarectal instillation of the TLR5 agonist flagellin(FliC) on CHS in adult naive wildtype mice was analyzed.RESULTS 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 appearance.CONCLUSION Altogether, these data suggest a pathophysiological continuum between intestinal dysbiosis and CHS, with a role for TLR5. | Geoffroy Mallaret Amandine Lashermes Mathieu Meleine Ludivine Boudieu Julie Barbier Youssef Aissouni Agathe Gelot Benoit Chassaing Andrew T Gewirtz Denis Ardid Frederic Antonio Carvalho | 2022 | World Journal of Gastroenterology2022，28，29： | 1 |
| 5 | Microbiota‐liver axis in hepatic disease显示文摘 | Benoit Chassaing Lucie Etienne‐Mesmin Andrew T. Gewirtz | 2014 | Hepatology2014，，1： | 1 |
| 6 | Bile salts induce long polar fimbriae expression favouring Crohn’s disease‐associated adherent‐invasive Escherichia coli interaction with Peyer’s patches显示文摘 | Benoit Chassaing Lucie Etienne‐Mesmin Richard Bonnet Arlette Darfeuille‐Michaud | 2012 | Environmental Microbiology2012，，2： | 1 |
| 7 | Crohn disease-associated adherent-invasive E. coli bacteria target mouse and human Peyer’s patches via long polar fimbriae显示文摘 | Chassaing Benoit Rolhion Nathalie de Vallée Amélie Salim Sa’ad Y Prorok-Hamon Maelle Neut Christel Campbell Batty J S?derholm Johan D Hugot Jean-Pierre Colombel Jean-Frédéric Darfeuille-Michaud Arlette | 2011 | Journal of Clinical Investigation2011，，3： | 1 |
| 8 | Bile salts induce long polar fimbriae expression favouring Crohn’s disease‐associated adherent‐invasive Escherichia coli interaction with Peyer’s patches显示文摘 | Benoit Chassaing Lucie Etienne‐Mesmin Richard Bonnet Arlette Darfeuille‐Michaud | 2012 | Environmental Microbiology2012，，2： | 1 |
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