Prostaglandin production by macrophages and the effect of anti-inflammatory drugs.
1 Macrophages derived from peritoneal cavity inflammatory exudates of guinea-pigs produced substantial amounts of prostaglandin E2-like activity during in vitro culture, so providing the basis for an experimental model of prostaglandin production during inflammatory reactions. 2 Dose-related inhibition of prostaglandin biosynthesis was demonstrated by 16 acidic non-steroidal anti-inflammatory drugs. 3 Seven anti-inflammatory glucocorticosteroid preparations inhibited prostaglandin production in a dose-related manner. The relative potencies of dexamethasone, prednisolone and hydrocortisone were consistent with clinical anti-inflammatory ranking. Cortisone, however, failed to inhibit macrophage prostaglandin production. 4 Three other agents used in the treatment of inflammatory joint diseases were examined. Sodium aurothiomalate inhibited prostaglandin production, although higher concentrations were toxic to macrophages. D-Penicillamine did not affect macrophage prostaglandin production. Colchicine, in contrast, enhanced prostaglandin production at some concentrations. 5 The probable significance of macrophages as a source of prostaglandins, during inflammatory responses, is discussed.
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D005938:Glucocorticoids / Q000494:pharmacology; D006168:Guinea Pigs; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D011453:Prostaglandins / Q000096:biosynthesis*; D011863:Radioimmunoassay; D012459:Salicylates / Q000494:pharmacology; D013997:Time Factors
D000893:Anti-Inflammatory Agents; D005938:Glucocorticoids; D011453:Prostaglandins; D012459:Salicylates; D007213:Indomethacin