Abstract
It is known that macrophages produce large amounts of eicosanoids during phagocytosis and that pharmacological concentrations of prostaglandin E 2 (PGE 2) inhibit phagocytosis in several models. However, the physiological effect on phagocytosis of endogenous prostaglandins, produced during CR1- or FcR-mediated bacterial phagocytosis, remains unclear. In this study, we show that indomethacin inhibits the CR1- but not the FcR-dependent phagocytosis of bacteria by rat peritoneal cells in the same range of concentrations that inhibit the synthesis of PGE 2, PGI 2 and thromboxane A 2. An exogenous supply of PGE 2 and PGE 1 (10 −10 to 10 −8 M) restored the CR1-mediated phagocytosis; higher concentrations were inhibitory. Our data indicate that PGE 2 and/or PGI 2, produced by rat periteneal cells, are involved in CR1-dependent bacterial phagocytosis.
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