PROSTAGLANDIN PRODUCTION BY MACROPHAGES AND THE EFFECT OF ANTI‐INFLAMMATORY DRUGS

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Abstract
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. Dose‐related inhibition of prostaglandin biosynthesis was demonstrated by 16 acidic non‐steroidal anti‐inflammatory drugs. 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. 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. The probable significance of macrophages as a source of prostaglandins, during inflammatory responses, is discussed.