Eicosanoids modulate CR1- and Fc-dependent bacterial phagocytosis.
It is known that macrophages produce large amounts of eicosanoids during phagocytosis and that pharmacological concentrations of prostaglandin E2 (PGE2) 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 PGE2, PGI2 and thromboxane A2. An exogenous supply of PGE2 and PGE1 (10(-10) to 10(-8) M) restored the CR1-mediated phagocytosis; higher concentrations were inhibitory. Our data indicate that PGE2 and/or PGI2, produced by rat peritoneal cells, are involved in CR1-dependent bacterial phagocytosis.
Coquette
A
A
Laboratoire d'Immunologie, Faculté de Médecine, Université Libre de Bruxelles, Brussels, Belgium.
Boeynaems
J M
JM
Vray
B
B
D000527:Alprostadil / Q000494:pharmacology; D000818:Animals; D015232:Dinoprostone / Q000494:pharmacology; D015777:Eicosanoids / Q000096:biosynthesis; D007213:Indomethacin / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects / Q000276:immunology*; D008297:Male; D008837:Micrococcus / Q000276:immunology; D010529:Peritoneal Cavity / Q000166:cytology; D010587:Phagocytosis / Q000187:drug effects*; D011453:Prostaglandins / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D017463:Receptors, Complement 3b / Q000276:immunology*; D011961:Receptors, Fc / Q000276:immunology*
D015777:Eicosanoids; D011453:Prostaglandins; D017463:Receptors, Complement 3b; D011961:Receptors, Fc; D000527:Alprostadil; D015232:Dinoprostone; D007213:Indomethacin