Bacteria, genetics and irritable bowel syndrome

Abstract

EVALUATION OF: Villani AC, Lemire M, Thabane M et al. Genetic risk factors for post-infectious irritable bowel syndrome following a waterborne outbreak of gastroenteritis. Gastroenterology 138, 1502-1513 (2010). While the pathogenesis of irritable bowel syndrome (IBS) remains to be fully defined, two clinical observations - the occurrence, de novo, of IBS following bacterial gastroenteritis and the history, commonly obtained from IBS patients, of other instances of the syndrome within their families - have instigated investigations, in IBS, of the potential roles, on the one hand, of the gut microbiota and the host response and, on the other hand, of genetic factors. The study reviewed here relates to both of these factors by studying genetic predisposition to postinfective IBS in a large population of individuals who were exposed to a multimicrobial enteric infection, which resulted in a severe outbreak of gastroenteritis and was followed by the development of IBS in over a third. In this detailed study, the investigators identified a number of genes that were linked significantly to the development of postinfectious-IBS in the Toll-like receptor 9, IL-6 and cadherin 1 regions. These genes play important roles in bacterial recognition, the inflammatory response and epithelial integrity, respectively, and provide considerable support for the hypothesis that links IBS onset to disturbances in the microbiota and the host response.

Breaking down the barriers: the gut microbiome, intestinal permeability and stress-related psychiatric disorders

“…However, individuals with pre-existing psychological disorders are known to be at an increased risk of developing post-infectious IBS (PI-IBS) in particular (Thabane and Marshall, 2009 ). Variations in several genes associated with bacterial recognition, the inflammatory response and epithelial integrity including TLR9, IL-6 and cadherin 1 genes have been identified as risk factors for the development of PI-IBS (Craig and Quigley, 2010 ; Villani et al, 2010 ). A longitudinal study which examined the rate of IBS development following an accidental outbreak of E. coli 0157:H7 into a town's (Walkerton) water supply identified an increased rate of IBS two years after the outbreak (Marshall, 2009 ).…”

Commensal bacteria

“…A variety of clinical and demographic factors have been shown to increase the risk for the development of IBS following bacterial gastroenteritis: female sex, past history of anxiety or depression, more severe clinical course of gastroenteritis and a persistent inflammatory response in the colonic mucosa. Most recently, some genetic factors which seem to predispose to PI-IBS have been identified [9 ]; interestingly, the genes implicated code for interleukins and epithelial barrier factors considered relevant to the pathogenesis of IBS, in general [10]. The ability of infectious agents, such as Clostridium difficile [11], to trigger relapses of existing IBD have been recognized for decades; what is new is the possibility that the onset of IBD, like IBS, may be triggered by an enteric infection [12].…”