Post-infectious irritable bowel syndrome:Mechanistic insights into chronic disturbances following enteric infection

Irritable bowel syndrome(IBS)is a commonly encountered chronic functional gastrointestinal(GI)disorder.Approximately 10%of IBS patients can trace the onset of their symptoms to a previous a bout of infectious dysentery.The appearance of new IBS symptoms following an infectious event is defined as po...

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Published inWorld journal of gastroenterology : WJG Vol. 20; no. 14; pp. 3976 - 3985
Main Authors Beatty, Jennifer K, Bhargava, Amol, Buret, Andre G
Format Journal Article
LanguageEnglish
Published United States Baishideng Publishing Group Co., Limited 14.04.2014
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Summary:Irritable bowel syndrome(IBS)is a commonly encountered chronic functional gastrointestinal(GI)disorder.Approximately 10%of IBS patients can trace the onset of their symptoms to a previous a bout of infectious dysentery.The appearance of new IBS symptoms following an infectious event is defined as post-infectiousIBS.Indeed,with the World Health Organization estimating between 2 and 4 billion cases annually,infectious diarrheal disease represents an incredible international healthcare burden.Additionally,compounding evidence suggests many commonly encountered enteropathogens as unique triggers behind IBS symptom generation and underlying pathophysiological features.A growing body of work provides evidence supporting a role for pathogen-mediated modifications in the resident intestinal microbiota,epithelial barrier integrity,effector cell functions,and innate and adaptive immune features,all proposed physiological manifestations that can underlie GI abnormalities in IBS.Enteric pathogens must employ a vast array of machinery to evade host protective immune mechanisms,and illicit successful infections.Consequently,the impact of infectious events on host physiology can be multidimensional in terms of anatomical location,functional scope,and duration.This review offers a unique discussion of the mechanisms employed by many commonly encountered enteric pathogens that cause acute disease,but may also lead to the establishment of chronic GI dysfunction compatible with IBS.
Bibliography:Jennifer K Beatty;Amol Bhargava;Andre G Buret;Department of Biological Sciences,University of Calgary
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Correspondence to: Andre G Buret, PhD, Professor, Department of Biological Sciences, University of Calgary, 2500 University Drive, NW, Calgary, AB T2N 1N4, Canada. aburet@ucalgary.ca
Telephone: +1-403-2202817  Fax: +1-403-2899311
Author contributions: Beatty JK, Bhargava A and Buret AG wrote this paper.
ISSN:1007-9327
2219-2840
DOI:10.3748/wjg.v20.i14.3976