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Research

 

Abdominal pain is a leading cause of morbidity in gastrointestinal disease. Despite this we still know little of how pain is triggered in “functional” gastrointestinal disorders such as irritable bowel syndrome (IBS), in which no overt clinical pathology can be detected. Furthermore, in organic diseases such as inflammatory bowel disease (IBD), previous assumptions that treating the inflammation would resolve the pain appear to be only partly true, with a significant proportion of patients reporting pain while in clinical remission.


One hypothesis supported by work from my lab and others, is that the bowel of IBS or IBD patients produces pro-nociceptive mediators capable of stimulating pain sensing nerves (nociceptors), which relay signals (nociception) to the brain where it is interpreted as pain. This process is referred to as peripheral sensitisation, and we believe it is an important cause of pain in patients with IBS and IBD. Using human tissue based approaches we have been able to identify a critical role for the voltage gated sodium channel subtype NaV1.9 in the activation of visceral nociceptors by pro-nociceptive mediators released from the bowel of IBS and IBD patients, and discovered a previously unrecognised role of Matrix Metalloproteinases in the activation of visceral nociceptors in IBD. Work now continues to further understand the mediators and mechanisms of peripheral sensitisation in gastrointestinal disease with an ultimate goal of developing effective visceral analgesics for the treatment of pain in IBS and IBD.