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.
The motility of the upper gastrointestinal tract in the interdigestive state shows a cycling pattern called Migrating Motor Complex (MMC) and is composed by phases I, II and III. Gastric, biliary and pancreatic secretion show cyclical fluctuations during fasting closely associated with the motor activity. The motor and secretory interdigestive activity is regulated by a complex interplay of nerval and humoral mechanisms. Among them, motilin, a gastrointestinal hormone mainly secreted from the duodenum, is supposed to play a central role in the initiation of phase III. Gastric acid secretion, directly or by means of motilin release, may modulate the duration of the MMC and the propagation of phase III in the small intestine. Pancreatic secretion does not initiate phase III but may exert a control on gastric interdigestive motility probably by means of pancreatic polypeptide release. Biliary interdigestive secretion seems to play a little or no role in the control of these phenomena. The coordination of motor and secretory events is likely to be under control of the duodenum.
