• 1 January 1982
    • journal article
    • research article
    • Vol. 49  (3) , 623-630
Abstract
The addition of prostaglandins E2(PGE2), PGD2, PGI2, 6-keto PGF1.alpha. and thromboxane B2 (TXB2) to human monocyte cultures, inhibited the production of the 2nd component of complement (C2). PGF2.alpha. did not significantly affect C2 production. As the former compounds, but not the latter increase intracellular cAMP, it was thought that the effect was mediated by this action. The addition of cyclo-oxygenase and lipoxygenase inhibitors [indomethacin, 5, 8, 11, 14-eicosatetraynoic acid] to monocyte cultures enhanced the synthesis of complement components and other proteins in a dose-dependent fashion: cyclo-oxygenase inhibitors being more potent in this regard than lipoxygenase inhibitors. The enhancing effect of cyclo-oxygenase inhibitors paralleled their ability to inhibit cyclo-oxygenase activity. The enhancement of C2 synthesis by the addition of cyclo-oxygenase and lipoxygenase inhibitors was reversed by the addition of PG to the cultures. Production of PG by monocytes could provide an endogenous mechanism to control the synthesis of complement components and other proteins.