Immunoreactive interleukin-1[beta] release from the rat gastric
fundus is reduced by glucocorticoids and inhibitors of gastric acid
secretion.
Montuschi, Paolo, Giuseppe Tringali, Adriana Mirtella, Luca Parente,
Enzo Ragazzoni, Paolo Preziosi, and Pierluigi Navarra.
Institutes of Pharmacology, School of Pharmacy, University of
Palermo, via Forlanini 1 - 90134 Palermo, and Catholic University
Medical School, Largo Francesco Vito 1 - 00168 Rome, Italy
APStracts 3:0021G, 1996.
Interleukin-1 (IL-1) is known to regulate gastric functions via a
central action at the hypothalamic level, and it has also been shown
that this cytokine can directly modulate rat gastric motility. This
study was conducted to determine whether IL-1[beta] is produced and
released by rat gastric fundi in vitro. IL-1[beta] immunoreactivity
was released in measurable amounts from explanted rat gastric tissue.
This release was not affected by electrical stimulation of the
gastric strips or by agents that induce IL-1 biosynthesis. It could
be inhibited only by the glucocorticoid, dexamethasone. Ex-vivo
experiments confirmed the inhibitory role of glucocorticoids and
showed that IL-1[beta] release can be inhibited by agents that reduce
gastric acid secretion, suggesting that the latter might stimulate
IL-1[beta] synthesis and release. In light of the well established
gastroprotection exerted by IL-1, H+-induced IL-1[beta] release might
serve as a protection against mucosal injuries caused by acid
secretion, and the inhibition of this release by glucocorticoids
might be involved in the pathogenesis of gastric damage associated
with severe stress or steroid therapy.
Received 9 March 1995; accepted in final form 16 January 1996.
APS Manuscript Number G103-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 29 January 96