Pronounced changes in gut neuropeptide content and innervation patterns have been observed in the inflamed intestine of patients with inflammatory bowel disease. It is not known to date whether these changes in neuropeptides are due to altered synthesis and release from intrinsic and/or extrinsic neurons and nerve fibers. The changes in circular smooth muscle response associated with diminished VIP in the intestine of patients with Crohn's disease suggests that VIP may play an important role in the pathophysiology of motility in IBD. The pronounced increase in SP receptors at small vessels in all gut layers and at lymph nodules in the inflamed intestine of IBD patients supports the hypothesis that SP is a modulator of inflammation in IBD and possibly acts by release from extrinsic sensory nerves of the gut. Sensory nerve may play a role not only in enhancing an inflammatory response in the intestine, but also in tissue repair. An inflammatory response after tissue injury and subsequent wound healing presumably is the normal response in healthy tissue. In IBD however, this sequence may be deeply disturbed by an unrestricted immune response which does not lead to or delays intestinal tissue healing. Although it is intriguing to postulate that interactions between the immune system and nervous system exist and play a role in the pathophysiology of intestinal inflammation, in vivo studies blocking or mimicking neuropeptide action are needed to prove this bidirectional communication.
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