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The putative role of the intestinal microbiota in the irritable bowel syndrome.

Abstract

The irritable bowel syndrome (IBS) is a chronic abdominal symptom complex that is heterogeneous in terms of its clinical presentation and underlying pathophysiology and pathogenesis. It is now established that enteric infection can trigger the syndrome in at least a subset of patients. In addition, there is growing evidence of low grade inflammation and immune activation in the distal bowel of some IBS patients. These observations now prompt the question as to what maintains gut dysfunction in these patients. The intestinal microbiota influences a broad array of host organs that include the gut and the brain, and is an important determinant of normal function in these systems. Disruption of the delicate balance between the host and its intestinal microbiota (termed dysbiosis) results in changes in the mucosal immune system that range from overt inflammation as seen in Crohn's Disease, to low grade inflammation without tissue injury, as seen in a subset of IBS patients. Under experimental conditions, disruption of the microbiota also produces changes in gut sensory-motor function and immune activity. Thus, dysbiosis induced by infection, dietary change or drugs such as antibiotics could produce low grade inflammation and chronic gut dysfunction, reminiscent of that seen in IBS. Fluctuations in gut physiology destabilize the habitat of commensal bacteria and provide a basis for chronic dysbiosis. Recent observations in animal models that changes in gut flora influence behavior provide a basis for a novel unifying hypothesis that accommodates both gut dysfunction and behavioral changes that characterize many IBS patients. This hypothesis states that dysbiosis exists in at least a subset of IBS patients, as a result of infection, dietary change or drugs and contributes to gut inflammatory and functional change in addition to psychiatric co-morbidity.

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  • Authors+Show Affiliations

    ,

    The Farncombe Digestive Health Research Institute, The Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada. scollins@mcmaster.ca

    , ,

    Source

    MeSH

    Animals
    Disease Models, Animal
    Enteric Nervous System
    Gastrointestinal Motility
    Gastrointestinal Tract
    Humans
    Immunity, Mucosal
    Inflammation
    Irritable Bowel Syndrome
    Risk Factors

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't
    Review

    Language

    eng

    PubMed ID

    19740713

    Citation

    Collins, S M., et al. "The Putative Role of the Intestinal Microbiota in the Irritable Bowel Syndrome." Digestive and Liver Disease : Official Journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver, vol. 41, no. 12, 2009, pp. 850-3.
    Collins SM, Denou E, Verdu EF, et al. The putative role of the intestinal microbiota in the irritable bowel syndrome. Dig Liver Dis. 2009;41(12):850-3.
    Collins, S. M., Denou, E., Verdu, E. F., & Bercik, P. (2009). The putative role of the intestinal microbiota in the irritable bowel syndrome. Digestive and Liver Disease : Official Journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver, 41(12), pp. 850-3. doi:10.1016/j.dld.2009.07.023.
    Collins SM, et al. The Putative Role of the Intestinal Microbiota in the Irritable Bowel Syndrome. Dig Liver Dis. 2009;41(12):850-3. PubMed PMID: 19740713.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - The putative role of the intestinal microbiota in the irritable bowel syndrome. AU - Collins,S M, AU - Denou,E, AU - Verdu,E F, AU - Bercik,P, Y1 - 2009/09/08/ PY - 2009/07/22/received PY - 2009/07/30/accepted PY - 2009/9/11/entrez PY - 2009/9/11/pubmed PY - 2010/1/27/medline SP - 850 EP - 3 JF - Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver JO - Dig Liver Dis VL - 41 IS - 12 N2 - The irritable bowel syndrome (IBS) is a chronic abdominal symptom complex that is heterogeneous in terms of its clinical presentation and underlying pathophysiology and pathogenesis. It is now established that enteric infection can trigger the syndrome in at least a subset of patients. In addition, there is growing evidence of low grade inflammation and immune activation in the distal bowel of some IBS patients. These observations now prompt the question as to what maintains gut dysfunction in these patients. The intestinal microbiota influences a broad array of host organs that include the gut and the brain, and is an important determinant of normal function in these systems. Disruption of the delicate balance between the host and its intestinal microbiota (termed dysbiosis) results in changes in the mucosal immune system that range from overt inflammation as seen in Crohn's Disease, to low grade inflammation without tissue injury, as seen in a subset of IBS patients. Under experimental conditions, disruption of the microbiota also produces changes in gut sensory-motor function and immune activity. Thus, dysbiosis induced by infection, dietary change or drugs such as antibiotics could produce low grade inflammation and chronic gut dysfunction, reminiscent of that seen in IBS. Fluctuations in gut physiology destabilize the habitat of commensal bacteria and provide a basis for chronic dysbiosis. Recent observations in animal models that changes in gut flora influence behavior provide a basis for a novel unifying hypothesis that accommodates both gut dysfunction and behavioral changes that characterize many IBS patients. This hypothesis states that dysbiosis exists in at least a subset of IBS patients, as a result of infection, dietary change or drugs and contributes to gut inflammatory and functional change in addition to psychiatric co-morbidity. SN - 1878-3562 UR - https://www.unboundmedicine.com/medline/citation/19740713/The_putative_role_of_the_intestinal_microbiota_in_the_irritable_bowel_syndrome_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1590-8658(09)00329-6 DB - PRIME DP - Unbound Medicine ER -