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.
Highlights
Inflammatory bowel disease (IBD) arises from complex interactions of genetic, environmental, and microbial factors [1]
There are at least three possible mechanisms that can drive pathogenic immunologic responses in Crohn’s disease (CD) to luminal microbes: (1) changes in microbial composition leading to dysbiosis, (2) functional alteration of commensal bacteria as described for Adherent and Invasive Escherichia coli (AIEC), toxigenic Bacteroides fragilis, Campylobacter and Helicobacter species or (3) involvement of traditional microbial pathogens such as Mycobacterium avium subspecies paratuberculosis
This is consistent with the abnormal expression of the tight junction-associated pore-forming claudin-2 protein at the plasma membrane of intestinal epithelial cells (IEC) observed in AIEC-infected mice [56]. This disruption allows the bacteria to penetrate into and beyond the epithelial monolayer triggering a chronic immune response. These findings provide a link between microbes related to IBD, disruption of the intestinal epithelial cell barrier, and disease pathogenesis [3,57]
Summary
Inflammatory bowel disease (IBD) arises from complex interactions of genetic, environmental, and microbial factors [1]. In contrast to infections with Citrobacter rodentium or Salmonella enterica serotype Typhimurium, which induce acute and self-limiting infections, H. hepaticus only causes disease in immunocompromised Rag2-deficient mice that lack immune regulation and mount inflammatory responses toward intestinal bacteria [18].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Journal of Gastrointestinal & Digestive System
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
