Dissociation of phagocytosis from stimulation of the oxidative metabolic burst in macrophages.

We explored the relationship between phagocytosis and the triggering of oxidative metabolism using resident, lipopolysaccharide (LPS)-elicited, and bacille Calmette-Guérin (BCG)-activated murine peritoneal macrophages. Sheep erythrocytes (E) coated with IgG [E(IgG)], E coated with IgM and complement [E(IgM)C], and E treated with 1% glutaraldehyde (GE) were used as stimuli. All three types of macrophages released superoxide anion (O2-) during phagocytosis of E(IgG). All macrophage types phagocytosed E(IgM)C and GE but none were stimulated to release O2- during phagocytosis of these particles. Vigorous consumption of oxygen was also stimulated by the ingestion of E(IgG) but not by ingestion of E(IgM)C or GE. E(IgM)C did not scavenge the O2- released from macrophages during phagocytosis of E(IgG) or during exposure to phorbol myristate acetate, and further addition of IgG anti-E antibody to E(IgM)C or GE permitted optimal stimulation of macrophage O2- release by these particles. The capacity of macrophages to ingest E(IgM)C and GE without stimulating the respiratory burst raises the possibility that clearance of particulate matter not opsonized with specific IgG might be achieved without stimulation of the release of toxic oxygen metabolites, and, therefore, without the risk of oxidative damage to the phagocytic cell or surrounding tissue.