Mechanisms Of Visceral Sensitization In Functional Gastrointestinal Disorder Evidence for Peripheral Sensitization

It is known that at least a third of patients with FGD have a previous history of gut inflammation or injury in the form of gastroenteritis or surgery (97). Although the majority of patients with such gut injury recover, a proportion go on to develop chronic symptoms such as pain or bowel dysfunction, this subgroup being labeled as having postinfectious IBS (PI-IBS).

The environment of nociceptor terminals in the gut of some patients with IBS is likely to be altered given the increased number of inflammatory cells that have been demonstrated in these patients. Increased gut permeability and altered mucosal characteristics, such as increased numbers of rectal mucosal enteroendocrine cells and T lymphocytes that have been documented in subjects with PI-IBS suggest a role for these peripheral mechanisms in the visceral hypersensitivity observed in these patients (98). Interleukin-1 P (IL-1P) is an important modulator of the inflammatory process, and greater expression of IL-1P mRNA has been reported in patients with PI-IBS both during and after gastroenteritis compared to individuals who did not subsequently develop PI-IBS and controls (99). Furthermore, some recent preliminary work has suggested that a proportion of IBS patients may be predisposed to prolonged inflammation due to reduced secretion of the counter inflammatory cytokines IL-10 and transforming growth factor-p. The frequency of the high producer alleles for both mediators was found to be significantly reduced in a proportion of IBS patients compared to controls. It was proposed that low secretors of these cytokines may be less efficient in down-regulating the response to inflammatory stimuli such as enteric infection (100).

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