THE ROLE OF THE HUMAN SYNOVIAL FIBROBLAST IN MONOSODIUM URATE CRYSTAL-INDUCED SYNOVITIS

  • 1 January 1983
    • journal article
    • research article
    • Vol. 10  (4) , 602-611
Abstract
Human synovial fibroblasts (HSF) were cultured to identify and quantitate-arachidonate metabolites released after exposure to monosodium urate (MSU) crystals. These crystals caused a significant release of PGE2 [prostaglandin E2] and 6-keto-PGF1.alpha.. Media lactate dehydrogenase levels from MSU-exposed HSF were equal to controls. Serum was required for the increase in metabolite release. Indomethacin and dexamethasone inhibited metabolite release, whereas colchicine increased metabolite release. MSU (1 mg/ml) released hydroxyeicosatetraenoic acids (HETE) from HSF whereas 20-fold higher doses were required to release these metabolites from human polymorphonuclear leukocytes. Colchicine increased but lipoxygenase inhibitors decreased HETE synthesis. Arachidonate metabolites from HSF may contribute to the pathogenesis of crystal-provoked synovitides.