The irritable bowel syndrome (IBS) may be defined as a painful chronic abdominal symptom complex which is usually associated with altered bowel habit, and for which there is no discernible underlying structural abnormality. It is generally accepted that symptoms are generated by abnormalities of gut function, including altered sensory perception, abnormal motility and, in some patients, abnormalities of epithelial function. Behavioural factors are important, particularly in the reporting of symptoms. What is lacking is an understanding of the pathogenetic mechanisms that alter gut function. IBS is a heterogeneous condition, not only in its clinical presentation and pathophysiology, but also in terms of its pathogenesis. While both central and peripheral factors have been implicated in the pathogenesis of IBS, this article will restrict itself to an evaluation of the evidence supporting inflammation as a basis for altered gut function in IBS.

In considering the role of inflammation in IBS, one is prompted to make a comparison with asthma. Like IBS, asthma was once considered a psychosomatic disorder, particularly in non-atopic children. For more than 50 years the treatment of asthma focused on the pharmacological correction of abnormal end organ physiology (that is, airways hyperresponsiveness), an approach that is similar to current therapeutic approaches to IBS, and which are aimed at modulating motor activity or sensory perception. The subsequent discovery of inflammatory cells in the normally sterile broncheoalveolar lavage led to the recognition of asthma as an inflammatory condition. There are two reasons why a similar shift in thinking in IBS will be difficult. Firstly, the gut is normally in a state of controlled inflammation and the challenge of identifying a subtle increase in inflammatory cell number or composition is not to be underestimated. Secondly, IBS is intuitively more heterogeneous than asthma, and inflammation is unlikely to be a factor in all …