Review Article
Importance of Bacteria as Trigger in Inflammatory Bowel Disease
Jérémy Denizot1,2, Nicolas Dreux1,2, Arlette Darfeuille-Michaud1,2,3 and Nicolas Barnich1,2,3* | |
1Clermont Université, M2iSH, Microbe intestin inflammation et Susceptibilité de l’Hôte, UMR 1071 Inserm/Université d’Auvergne, France | |
2Unité Sous Contrat Institut National de la Recherche Agronomique 2018, Clermont-Ferrand F-63001, France | |
3Institut Universitaire de Technologie, Génie Biologique, Aubière F-63172, France | |
Corresponding Author : | Nicolas Barnich M2iSH, Inserm/Université d’Auvergne UMR 1071 CBRV, 28 place Henri Dunant 63001 Clermont-Ferrand, France Tel: (33)4-73-17-83-76 Fax: (33)4-73-17-83-71 E-mail: nicolas.barnich@u-clermont1.fr |
Received January 06, 2012; Accepted February 03, 2012; Published February 05, 2012 | |
Citation: Denizot J, Dreux N, Michaud AD, Barnich N (2012) Importance of Bacteria as Trigger in Inflammatory Bowel Disease. J Gastroint Dig Syst S8:003. doi:10.4172/2161-069X.S8-003 | |
Copyright: © 2012 Denizot J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
Abstract
Inflammatory bowel diseases (IBD) provide a complex model of host-microbe interactions underpinning disease pathogenesis. Although there is no widespread agreement on the aetiology of IBD, there is evidence that microorganisms lead to the often severe inflammatory response characteristic of the disease. IBD is thought to result from an inappropriate and continuing inflammatory response to pathobionts microbes in a genetically susceptible host. In this review, we discuss the complex microbial ecosystem of the mammalian gut, the underlying genetic factors that predispose to IBD, and how these gene variants may alter host-microbe interactions and propagate inflammation. Incentive should be given to research that will promote a better understanding of host-microbial interactions in the intestine and lay the foundations for new therapeutic approaches to both treat and prevent onset and relapse of intestinal inflammation in genetically susceptible hosts.