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Eicosanoids modulate CR1- and Fc-dependent bacterial phagocytosis
A Coquette1, J M Boeynaems, B Vray
1Laboratoire d'Immunologie, Faculté de Médecine, Université Libre de Bruxelles, Brussels, Belgium.
Abstract:
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.
Insights
Endogenous prostaglandins, like prostaglandin E2 (PGE2), play a role in CR1-dependent bacterial phagocytosis by macrophages. Indomethacin
Area of Science:
- Immunology
- Cell Biology
- Prostaglandin Biology
Background:
- Macrophages produce eicosanoids during phagocytosis.
- Pharmacological doses of prostaglandin E2 (PGE2) inhibit phagocytosis.
- The role of endogenous prostaglandins in CR1- or FcR-mediated phagocytosis is unclear.
Purpose of the Study:
- To investigate the physiological role of endogenous prostaglandins in CR1- and FcR-dependent bacterial phagocytosis.
- To determine the effect of prostaglandin synthesis inhibition on phagocytosis.
Main Methods:
- Treatment of rat peritoneal cells with indomethacin, a prostaglandin synthesis inhibitor.
- Assessment of CR1- and FcR-dependent bacterial phagocytosis.
- Restoration of phagocytosis with exogenous prostaglandin E2 (PGE2) and E1.
Main Results:
- Indomethacin inhibited CR1-dependent phagocytosis at concentrations that also inhibited prostaglandin E2 (PGE2), PGI2, and thromboxane A2 synthesis.
- FcR-dependent phagocytosis was not affected by indomethacin.
- Exogenous PGE2 and PGE1 (10(-10) to 10(-8) M) restored CR1-mediated phagocytosis, while higher concentrations were inhibitory.
Conclusions:
- Endogenous prostaglandins, specifically PGE2 and/or PGI2, produced by rat peritoneal cells, are involved in CR1-dependent bacterial phagocytosis.
- The findings highlight a regulatory role for prostaglandins in specific phagocytic pathways.