Endogenous glucocorticoids inhibit neutrophil recruitment to
inflammatory sites in cholestatic rats.
Tjandra, Kartika, Paul Kubes, Kevin Rioux, and Mark G. Swain.
Gastrointestinal Research Group, Department of Medical Physiology,
University of Calgary, Calgary, Alberta, Canada T2N 4N1
APStracts 2:0249G, 1995.
Since glucocorticoids have been shown to inhibit leukocyte
accumulation to inflammatory sites (6,9), and endogenous
glucocorticoid levels are elevated in our cholestatic rat model, we
investigated their role during acute inflammation. Sprague-Dawley
rats (150-200g) were either bile duct resected (BDR) or sham resected
(sham). Five days later, a 2% carrageenan solution in saline was
injected s.c. into preformed air pouches on their backs. Animals were
sacrificed five hours later, and inflammatory response was
quantitated by measuring the exudate volume, cell count, and
myeloperoxidase (mainly in neutrophils) activity. We also pretreated
BDR/sham rats with RU486 (2mg/kg, ip), a glucocorticoid receptor
antagonist, 1 hour before carrageenan injection. BDR rats exhibited
an impaired inflammatory response reflected by 20%, 52% and 42%
decreases in exudate volume, cell count and myeloperoxidase activity,
respectively (all p<0.05). RU486 treatment significantly
increased the inflammatory response in BDR rats (to sham levels), but
not in sham rats. These results suggest that endogenous
glucocorticoid suppresses the inflammatory response in BDR rats.
Received 17 August 1995; accepted in final form 20 November 1995.
APS Manuscript Number G359-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95