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The classical scenario depicting irritable bowel syndrome (IBS) as a disturbance of the psychological sphere, accompanied by gut sensory and motor dysfunction, is being enriched by the identification of previously unrecognised peripherally acting molecular factors.
The relatively recent identification that IBS can be triggered in previously healthy individuals by a bout of infectious gastroenteritis (ie, post-infectious IBS) is a clear paradigm of the participation of biological factors in the pathogenesis of IBS.1 Abnormal metabolism of the important gut neurotransmitter serotonin (5-HT), tissue immune activation, increased mucosal permeability and changes in gut microbiota are other examples of the recent discoveries obtained by application of a molecular approach to IBS research.2 The identified cellular and molecular factors have been found to impact on the sensory and motor apparatus of the gut and, for certain aspects, they were associated with patients’ symptoms. For example, activated mast cells in proximity to colonic nerves correlated with abdominal pain in patients with IBS.3 Furthermore, application of extracts derived from colonic mucosal biopsies of IBS patients, but not healthy controls, to the gut of naive murine laboratory animals evoked increased activation of pain-related visceral pathways4 and an “IBS-like” visceral hyperalgesia.5
Sceptical observers would argue that such subtle abnormalities could hardly explain the complexity and protean manifestations of IBS symptoms. Indeed, “stress-related” factors continue to be important players in …
Competing interests: None.
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