Pharmacology of human spontaneous monocyte-mediated cytotoxicity. I. Enhancement by salicylates and steroids.
The effect of various antiinflammatory agents on the spontaneous cytotoxicity of human mononuclear cells in vitro was assessed. Acetylsalicylic acid (ASA) and hydrocortisone enhanced spontaneous monocyte-mediated cytotoxicity compared to control values. This enhancement could not be mediated through inhibition of prostaglandin biosynthesis since indomethacin had no effect on cytotoxic function and since the direct addition of PGE2 to the cell cultures did not inhibit the expression of cytotoxicity. Likewise, salicylic acid (SA), which had no effect on prostaglandin biosynthesis, also enhanced monocyte cytotoxicity. Stimulation of monocyte-mediated cytotoxicity resulting in more efficient antigen removal and thus decreasing antigen persistence may be an additional mechanism by which ASA, SA, and hydrocortisone modulate the destructive inflammatory response in rheumatoid arthritis.
D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001241:Aspirin / Q000494:pharmacology; D003602:Cytotoxicity, Immunologic / Q000187:drug effects*; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology*; D007213:Indomethacin / Q000494:pharmacology; D007694:Killer Cells, Natural / Q000502:physiology; D009000:Monocytes / Q000187:drug effects*; D011458:Prostaglandins E / Q000494:pharmacology; D012459:Salicylates / Q000494:pharmacology*
D000893:Anti-Inflammatory Agents; D011458:Prostaglandins E; D012459:Salicylates; D001241:Aspirin; D006854:Hydrocortisone; D007213:Indomethacin