Topic Highlight
Copyright ©2011 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Feb 7, 2011; 17(5): 557-566
Published online Feb 7, 2011. doi: 10.3748/wjg.v17.i5.557
Intestinal microbiota in inflammatory bowel disease: Friend of foe?
Francesca Fava, Silvio Danese
Francesca Fava, Silvio Danese, Inflammatory Bowel Disease Unit, Istituto Clinico Humanitas, Via Manzoni 113, 20089 Rozzano, Milano, Italy
Author contributions: Fava F and Danese S both generated the ideas and contributed to the writing of this manuscript.
Correspondence to: Silvio Danese, MD, PhD, Inflammatory Bowel Disease Unit, Istituto Clinico Humanitas, Via Manzoni 113, 20089 Rozzano, Milano, Italy. silvio.danese@humanitas.it
Telephone: +39-2-82244771 Fax: +39-2-82245101
Received: June 28, 2010
Revised: August 18, 2010
Accepted: August 25, 2010
Published online: February 7, 2011
Abstract

Inflammatory bowel disease (IBD) arises from disruption of immune tolerance to the gut commensal microbiota, leading to chronic intestinal inflammation and mucosal damage in genetically predisposed hosts. In healthy individuals the intestinal microbiota have a symbiotic relationship with the host organism and possess important and unique functions, including a metabolic function (i.e. digestion of dietary compounds and xenobiotics, fermentation of undigestible carbohydrates with production of short chain fatty acids), a mucosal barrier function (i.e. by inhibiting pathogen invasion and strengthening epithelial barrier integrity), and an immune modulatory function (i.e. mucosal immune system priming and maintenance of intestinal epithelium homeostasis). A fine balance regulates the mechanism that allows coexistence of mammals with their commensal bacteria. In IBD this mechanism of immune tolerance is impaired because of several potential causative factors. The gut microbiota composition and activity of IBD patients are abnormal, with a decreased prevalence of dominant members of the human commensal microbiota (i.e. Clostridium IXa and IV groups, Bacteroides, bifidobacteria) and a concomitant increase in detrimental bacteria (i.e. sulphate-reducing bacteria, Escherichia coli). The observed dysbiosis is concomitant with defective innate immunity and bacterial killing (i.e. reduced mucosal defensins and IgA, malfunctioning phagocytosis) and overaggressive adaptive immune response (due to ineffective regulatory T cells and antigen presenting cells), which are considered the basis of IBD pathogenesis. However, we still do not know how the interplay between these parameters causes the disease. Studies looking at gut microbial composition, epithelial integrity and mucosal immune markers in genotyped IBD populations are therefore warranted to shed light on this obscure pathogenesis.

Keywords: Microbiota; Inflammatory bowel disease; Microbial dysbiosis; Immune tolerance; Innate immunity; Mucosal barrier