A role for inflammation in irritable bowel syndrome?

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.

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Figure 1

Working hypothesis on the role of low grade inflammation in the pathogenesis of irritable bowel syndrome. A wide array of factors (for example, previous episodes of infective gastroenteritis, genetic factors, food allergies, and altered intestinal microflora) evoke mucosal low grade inflammation which is capable of sensitising both intrinsic primary afferent neurones (IPANs) and extrinsic primary afferent neurones. Abnormal stimulation of IPANs leads to altered intestinal motor function while sensitisation of extrinsic primary afferent neurones evokes visceral hypersensitivity and symptom generation. CNS, central nervous system.