Abstract
For about 40 years, nerves in the wall of the intestine have been postulated to play a role in the pathogenesis of inflammatory bowel disease (IBD). Storsteen and colleagues1 were the first to demonstrate that enteric neurons were involved in this process, by providing histological evidence for an increased number of myenteric ganglion cells in chronic ulcerative colitis. Similar observations were also made in Crohn’s disease2. Extrinsic nerves innervating the bowel have also been implicated in these diseases, based not only on the common observation of abdominal pain in IBD but also on clinical observations that vagotomy and pelvic nerve lesions could modify, and in some cases ‘improve’, the outcome of IBD3–5. Additionally, autonomic neuropathy has been described in IBD and might contribute to the symptoms of these diseases6,7. Though surgical denervation is no longer used for the therapeutic management of IBD, the role of nerves in this multifactorial disease has become established. This review will focus on human and animal studies on the role of nerves in intestinal inflammation. Consideration will be given to two possible ways that nerves are involved in IBD. First, through the local release of transmitters nerves may play a role in the development or maintenance of inflammation. Second, once initiated (by whatever means), the processes of inflammation could cause disruption of the normal pattern of innervation and the interactions of nerves and their target tissues. Finally, acknowledgement of the role of the central nervous system in modulation of immune function must be made, but it is outside the scope of this review to consider this aspect of the nervous regulation of inflammation.KeywordsMast CellInflammatory Bowel DiseaseUlcerative ColitisVasoactive Intestinal PeptideVasoactive Intestinal PolypeptideThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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