rss
Gut 2002;51:i41-i44 doi:10.1136/gut.51.suppl_1.i41
  • Papers

A role for inflammation in irritable bowel syndrome?

  1. G Barbara,
  2. R De Giorgio,
  3. V Stanghellini,
  4. C Cremon,
  5. R Corinaldesi
  1. Department of Internal Medicine and Gastroenterology, University of Bologna, Bologna, Italy
  1. Correspondence to:
    Dr G Barbara, Department of Internal Medicine and Gastroenterology, St Orsola Hospital, Via Massarenti 9, I-40138 Bologna, Italy;
    gbarbara{at}med.unibo.it

    Abstract

    Attention has been directed to the putative role of low grade mucosal inflammation in irritable bowel syndrome (IBS) on the basis of evidence showing that some patients with IBS have an increased number of inflammatory cells in the colonic and ileal mucosa. Previous episodes of infectious enteritis, genetic factors, undiagnosed food allergies, and changes in bacterial microflora may all play a role in promoting and perpetuating this low grade inflammatory process. Human and animal studies support the concept that inflammation may perturb gastrointestinal reflexes and activate the visceral sensory system even when the inflammatory response is minimal and confined to the mucosa. Thus abnormal neuroimmune interactions may contribute to the altered gastrointestinal physiology and hypersensitivity that underlies IBS. A brief review of the human and animal studies that have focused on the putative role of intestinal inflammation and infections in the pathogenesis of IBS is given.

    Register for free content

    The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.

    Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.