Potent inhibition of gastric acid secretion and ulcer formation by centrally and peripherally administered interleukin-1.

IL-1 beta is one of the most potent centrally acting inhibitors of gastric acid secretion in rats. Sites of action have been located in the anterior/preoptic area and paraventricular nucleus of the hypothalamus where other biological activities of IL-1 have also been described. IL-1 beta action is, so far, quite unique to this cytokine and its action is not reproduced by IL-2 or TNF alpha. The IL-1 effect involves prostaglandin pathways and is unrelated to CRF. Similarly, systemic injection of IL-1 induces a long lasting inhibition of acid secretion through prostaglandin-dependent mechanisms. Several findings support the possibility that the effect of systemic IL-1 can be CNS-mediated and/or exerted at the periphery through local release of PG in the stomach. Exogenous IL-1 given into either the circulation or the cerebrospinal fluid also inhibits gastric injury induced by a variety of experimental models (stress, aspirin, ethanol). Such a protective effect is mediated through the inhibition of acid secretion and prostaglandin release, although other mechanisms may also contribute. Whether endogenously released IL-1 beta exerts a protective role in the gastric mucosa is still to be investigated.