LIPOPOLYSACCHARIDE-INDUCED SUPPRESSION OF ERYTHROCYTE BINDING AND PHAGOCYTOSIS VIA FC-GAMMA-RI, FC-GAMMA-RII, FC-GAMMA-RIII, AND CR3 RECEPTORS IN MURINE MACROPHAGES

In this study we have investigated the ability of lipopolysaccharide ( LPS) to suppress binding and phagocytosis of erythrocytes via various receptors on mouse macrophages. Thioglycollate-elicited peritoneal mac rophages were treated in vitro with LPS and the ability to bind and ph agocytose radiolabeled sheep red blood cells was determined. We show t hat LPS can directly suppress phagocytosis of immunoglobulin G-opsoniz ed and nonopsonized sheep red blood cells (SRBCs) by inflammatory macr ophages. Suppression was dose dependent and was observed after 4 h of exposure. This effect lasted for at least 24 h following the removal o f LPS. LPS suppressed the binding, rate, and absolute level of phagocy tosis via Fc receptors. Phagocytosis via all Fc receptors (FcgammaRI, FcgammaRII, and FcgammaRIII) was suppressed by LPS. Furthermore, suppr ession was not limited to Fc receptor-mediated phagocytosis because bi nding and uptake of C3bi-opsonized SRBCs to CR3 receptors was also dec reased following LPS treatment. LPS did not exert its effects via the production of interleukin-1 (IL-1), IL-6, tumor necrosis factor alpha, or interferon alpha/beta, because antibodies to these cytokines did n ot abrogate the effect. The ability of LPS to suppress binding and pha gocytosis of microorganisms may contribute to the toxic effects of LPS during gram-negative sepsis by preventing or delaying elimination of bacteria by host macrophages.