Microbiota-host interactions in irritable bowel syndrome: Epithelial barrier, immune regulation and brain-gut interactions Review uri icon

Overview

MeSH Major

  • Bacteria
  • Brain
  • Immunity, Mucosal
  • Intestinal Mucosa
  • Intestines
  • Irritable Bowel Syndrome
  • Microbiota

abstract

  • Irritable bowel syndrome (IBS) is a common, sometimes debilitating, gastrointestinal disorder worldwide. While altered gut motility and sensation, as well as aberrant brain perception of visceral events, are thought to contribute to the genesis of symptoms in IBS, a search for an underlying aetiology has, to date, proven unsuccessful. Recently, attention has been focused on the microbiota as a possible factor in the pathogenesis of IBS. Prompted by a number of clinical observations, such as the recognition of the de novo development of IBS following enteric infections, as well as descriptions of changes in colonic bacterial populations in IBS and supported by clinical responses to interventions, such as antibiotics and probiotics, that modify the microbiota, various approaches have been taken to investigating the microbiota-host response in IBS, as well as in animal models thereof. From such studies a considerable body of evidence has accumulated to indicate the activation or upregulation of both factors involved in bacterial engagement with the host as well host defence mechanisms against bacteria. Alterations in gut barrier function, occurring in response, or in parallel, to changes in the microbiota, have also been widely described and can be seen to play a pivotal role in generating and sustaining host immune responses both within and beyond the gut. In this manner a plausible hypothesis, based on an altered microbiota and/or an aberrant host response, for the pathogenesis, of at least some instances of IBS, can be generated.

publication date

  • January 2014

Research

keywords

  • Review

Identity

Language

  • eng

PubMed Central ID

  • PMC4112904

Digital Object Identifier (DOI)

  • 10.3748/wjg.v20.i27.8859

PubMed ID

  • 25083059

Additional Document Info

start page

  • 8859

end page

  • 66

number

  • 27