The present study evaluated whether macrophage activation would reduce the depression in the capacity of macrophages to produce H2O2 following EIgG phagocytosis. Macrophage activation was accomplished by exposing inflammatory rat peritoneal macrophages to 10 units of IFNγ for 72 h. IFNγ treatment caused a four to fivefold increase in phorbol myristate acetate (PMA)-triggered H2O2 production, but Fc receptor phagocytic function was unaltered. IFNγ-activated macrophages were able to phagocytize a greater number of EIgG before a decrease in PMAtriggered H2O2 production was observed and the level of H2O2 production did not fall below that of untreated-inflammatory macrophages that had not received an EIgG phagocytic challenge. The depression in Fc receptor phagocytic function was unaltered with macrophage activation. These results indicate that activated macrophages are resistant to the depression of respiratory burst capacity caused by erythrocyte phagocytosis and suggests that IFNγ treatment may be effective in preventing the impairment of host defense against bacterial infection that is associated with erythrocyte phagocytosis.
ASJC Scopus subject areas
- Immunology and Allergy