Our previous studies have shown that the phagocytosis of IgG-coated erythrocytes (EIgG) in vivo increases the mortality rate with bacterial infection, and EIgG phagocytosis in vitro depresses phorbol myristate acetate (PMA)-triggered H2O2 production. The present study was undertaken to determine if the depression of H2O2 production caused by EIgG phagocytosis could be reversed by exposing macrophages to priming agents. Macrophages exposed to 100 μg/ml of C. parvum, it's pyridine-soluble extract (PE), or the pyridine extract residue (PER) for 1 hr showed an enhanced production of H2O2 in response to PMA triggering. The priming effect of C. parvum, PE, and PER lasted for 3-6 hr. 18 hr after exposure to C parvum or PER, PMA-triggered H2O2 production was depressed, however PE did not have this effect. The priming effect of C parvum was not prevented by cycloheximide. EIgG phagocytosis caused a dose dependent depression of PMA-triggered H2O2 production. When macrophages were exposed to C. parvum, PE, or PER following EIgG phagocytosis, the priming of PMA-triggered H2O2 production was reduced but H2O2 production was maintained at levels equal to or greater than that of control macrophages. These results show that phagocytosis did not prevent the action of priming agents on macrophage respiratory burst capacity, and suggests that such agents may preserve macrophage bactericidal function following phagocytosis.
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