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Monosodium Urate Microcrystals Induce Cyclooxygenase-2 in Human
Monocytes
Marc Pouliot,
Michael J. James,
Shaun R. McColl,
Paul H. Naccache, and
Leslie G. Cleland
From the Rheumatology Unit, Royal Adelaide Hospital, Adelaide;
Department of Microbiology and Immunology, The University of Adelaide,
Adelaide, South Australia; Centre de Recherche en
Rhumatologie et Immunologie, Centre de Recherche du CHUL, Laval
University, Ste-Foy, Québec, Canada.
The formation and deposition of monosodium urate (MSU) microcrystals
in articular and periarticular tissues is the causative agent of acute
or chronic inflammatory responses known as gouty arthritis. Mononuclear
phagocyte activation is involved in early triggering events of gout
attacks. Because stimulated mononuclear phagocytes can constitute an
important source of the inducible isoform of cyclooxygenase (COX-2), we
evaluated the effects that proinflammatory microcrystals might have on
COX-2 protein expression in crystal-stimulated monocytes. We found that
MSU crystals, but not calcium pyrophosphate dihydrate (CPPD) crystals,
induced COX-2, which correlated with the synthesis of prostaglandin
E2 (PGE2) and thromboxane A2
(TXA2). Crystal-induced de novo synthesis of COX-2 was
dependent on transcriptional and translational events. Inhibition of
tyrosine phosphorylation, by herbimycin A, blocked crystal-induced COX-2. Similarly, an inhibitor of the p38
mitogen-activated protein kinase, SB 203580, inhibited the stimulation
of COX-2. Colchicine inhibited crystal-induced COX-2. In all cases,
prostanoid synthesis was concomitantly inhibited. Taken together, these
results implicate COX-2 in the development of MSU-induced inflammation.
Blood, Vol. 91 No. 5 (March 1), 1998:
pp. 1769-1776
© 1998 by The American Society of Hematology.
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