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a Department
of Biochemical Pharmacology, The William Harvey Research Institute,
Charterhouse Square, London EC1M 6BQ, UK, b Department of Gastroenterology, Institut
d'Investigacions Biomedique AP Sunyer, Hospital Clínic, Barcelona,
Spain, c Department of Molecular and Cellular Physiology,
LSU Medical Center, Shreveport, Louisiana, USA
Correspondence to: Dr Perretti.
Accepted for publication 30 March 1999
BACKGROUND
A previous study
showed that the glucocorticoid dexamethasone, at doses of 100 µg/kg
and above, inhibited leucocyte adhesion to rat mesenteric postcapillary
venules activated with interleukin 1
(IL-1), as assessed by videomicroscopy.
AIMSTo identify whether the
adhesion molecule, intercellular adhesion molecule 1 (ICAM-1), or the
chemokine KC could be targeted by the steroid to mediate its
antiadhesive effect.
METHODSRat mesenteries were
treated with IL-1 (20 ng intraperitoneally) and the extent of
leucocyte adhesion measured at two and four hours using intravital
microscopy. Rats were treated with dexamethasone, and passively
immunised against ICAM-1 or KC. Endogenous expression of these two
mediators was validated by immunohistochemistry, ELISA, and the
injection of specific radiolabelled antibodies.
RESULTSDexamethasone greatly
reduced IL-1 induced leucocyte adhesion, endothelial expression of
ICAM-1 in the postcapillary venule, and release of the mast cell
derived chemokine KC. Injection of specific antibodies to the latter
mediators was also extremely effective in downregulating (>80%)
IL-1 induced leucocyte adhesion.
CONCLUSIONSInduction by
IL-1 of endogenous ICAM-1 and KC contributes to leucocyte
adhesion to inflamed mesenteric vessels. Without excluding other
possible mediators, these data clearly show that dexamethasone interferes with ICAM-1 expression and KC release from mast cells, resulting in suppression of leucocyte accumulation in the bowel wall,
which is a prominent feature of several gastrointestinal pathologies.
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