The effect of bacterial lipopolysaccharide on the Fc-receptor-mediated respiratory burst in murine peritoneal macrophages has been examined. After treatment overnight with small quantities of LPS, macrophages exhibited dramatic diminution of their capacity to generate and secrete H2O2 when triggered with immune complexes. The effect of LPS treatment was dependent on the state of macrophage functional activation; only cells that were primed or fully activated in vivo or were treated with interferon-gamma in vitro were sensitive to this effect of LPS. The LPS-mediated loss of secretory function was both dose and time dependent and could be reproduced with the lipid A moiety of LPS. The effect was selective for H2O2 secretion triggered through the Fc receptor; the respiratory burst stimulated by phorbol diesters remained unaltered. Furthermore, LPS treatment did not alter either binding or ingestion of radiolabeled immune complexes in parallel with the change in H2O2 secretion, indicating that the suppressive effect was not due to compromised endocytic function. These results indicate that LPS treatment of primed macrophages regulates the function of Fc receptors and may uncouple receptor occupancy from generation and secretion of H2O2.

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