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Irritable bowel syndrome (IBS) is a common, functional gastrointestinal disorder, which affects approximately 10?20% of the general population.1?3 Despite its high prevalence, the pathogenesis of IBS is still very little understood, and seems to be multi-factorial disease.1?3 Many factors have been proposed to contribute to the pathogenesis of IBS, including visceral hypersensitivity, gastrointestinal dysmotility, activation of mucosal immune system, alterations of the gut microbiota, and impaired intestinal barrier function, as well as psychosocial distress.1?3 Recently, a newly identified cause for IBS is infectious gastroenteritis.1?3 About 10% of patients with IBS develop the symptoms consistent with diarrhea-predominant IBS (IBS-D) after an episode of infectious gastroenteritis and these patients are designated as postinfectious IBS (PI-IBS).4?6 Jalanka-Touvinene et al7 investigated the alteration of fecal microbiota composition and its association with clinical features in patients with PI-IBS. Compositional analysis of fecal microbiota showed the 27 discriminant bacterial groups, providing an index of microbial dysbiosis (IMD), which significantly separated the fecal microbial profile of PI-IBS patients from that of healthy control (HC), and the fecal microbiota of PI-IBS resembled that of IBS-D. The major differences in the fecal microbiota of PI-IBS compared to HC were the increase of the several members of Bacteroides and decrease of uncultured Clostridiales compared with HC. These descriminant microbial profiles, creating IMD positively correlated with intestinal symptoms, but not psychological symptoms. Also, IMD correlated with host mucosal gene expression including amino acid synthesis for gut integrity, cell junction pathways and inflammatory cytokine production, indicative of an increased inflammatory response and impaired intestinal barrier function in PI-IBS. The authors concluded that the fecal microbiota composition of patients with PI-IBS differs from that of HC, and resembles that of IBS-D. Host-microbe associations between host gene expression and altered fecal microbiota suggest that impaired intestinal barrier function may underlie both immunological and microbiological deviations in the pathogenesis of PI-IBS.
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