Depression of macrophage respiratory burst capacity and arachidonic acid release after Fc receptor-mediated phagocytosis.

The phagocytosis of IgG-coated erythrocytes (ElgG) by macrophages results in a subsequent depression of macrophage phagocytic function, respiratory burst capacity, and bactericidal activity. Our study was carried out to determine the importance of impaired arachidonic acid release in the depression of the respiratory burst after ElgG phagocytosis. The depression of triggered H2O2 production after ElgG phagocytosis was not due to cyclooxygenase products because indomethacin or aspirin did not modify the depression. Further studies revealed that the depression of triggered H2O2 production after ElgG phagocytosis was associated with a depression in the ability of macrophages to release arachidonic acid in response to PMA, zymosan, or calcium ionophore. The addition of exogenous arachidonic acid partially prevented the depression of triggered H2O2 production after ElgG phagocytosis. Unlike phagocytosis mediated by FcR, complement receptor-mediated phagocytosis did not alter H2O2 production or arachidonic acid release. Ligation of FcR was not sufficient to depress triggered H2O2 production and arachidonic acid release because these functions were not depressed when phagocytosis was inhibited with cytochalasin D. Thus, it was found that the depression of triggered H2O2 production by macrophages after FcR-mediated phagocytosis was associated with impaired release of arachidonic acid and that H2O2 production could be partially restored by the addition of arachidonic acid. These results suggest that the impairment of arachidonic acid release after FcR-mediated phagocytosis contributes to the depression of macrophage respiratory burst capacity after FcR-mediated phagocytosis.