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Aliment Pharmacol Ther. 2014 May;39(10):1033-42. doi: 10.1111/apt.12728. Epub 2014 Mar 25.

Review article: evidence for the role of gut microbiota in irritable bowel syndrome and its potential influence on therapeutic targets.

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1
St Luke's Medical Center, and Baylor College of Medicine, The University of Texas School of Public Health, Houston, TX, USA.

Abstract

BACKGROUND:

Irritable bowel syndrome (IBS) is a prevalent gastrointestinal disease with a substantial social and economic burden. Treatment options remain limited and research on the aetiology and pathophysiology of this multifactorial disease is ongoing.

AIM:

To discuss the potential role of gut microbiota in the pathophysiology of IBS and to identify possible interactions with pathophysiologic targets in IBS.

METHODS:

Articles were identified via a PubMed database search ['irritable bowel syndrome' AND (anti-bacterial OR antibiotic OR flora OR microbiota OR microflora OR probiotic)]. English-language articles were screened for relevance. Full review of publications for the relevant studies was conducted, including additional publications that were identified from individual article reference lists.

RESULTS:

The role of gut microbiota in IBS is supported by varying lines of evidence from animal and human studies. For example, post-infectious IBS in humans is well documented. In addition, certain probiotics and nonsystemic antibiotics appear to be efficacious in the treatment of IBS. Mechanisms involved in improving IBS symptoms likely go beyond mere changes in the composition of the gut microbiota, and accumulating animal data support the interplay of microbiota with other IBS targets, such as the gut-brain axis, visceral hypersensitivity, mucosal inflammation and motility.

CONCLUSION:

The role of the gut microbiota is still being elucidated; however, it appears to be one of several important factors that contributes to the aetiology and pathophysiology of the irritable bowel syndrome.

PMID:
24665829
DOI:
10.1111/apt.12728
[Indexed for MEDLINE]
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