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Lipopolysaccharide‐induced suppression of erythrocyte binding and phagocytosis via FCγRI, FCγRII, FCγRIII, and CR3 receptors in murine macrophages
Author(s) -
Sundaram Ramani,
O'Connor Maeve,
Cicero Mary,
Ghaffar Abdul,
Gangemi J. David,
Mayer Eugene R
Publication year - 1993
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.54.1.81
Subject(s) - phagocytosis , lipopolysaccharide , biology , receptor , macrophage , immunology , microbiology and biotechnology , neutrophile , fc receptor , inflammation , biochemistry , in vitro
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 macrophages were treated in vitro with LPS and the ability to bind and phagocytose radiolabeled sheep red blood cells was determined. We show that LPS can directly suppress phagocytosis of immunoglobulin G‐opsonized and nonopsonized sheep red blood cells (SRBCs) by inflammatory macrophages. Suppression was dose dependent and was observed after 4 h of exposure. This effect lasted for at least 24 h following the removal of LPS. LPS suppressed the binding, rate, and absolute level of phagocytosis via Fc receptors. Phagocytosis via all Fc receptors (FcγRI, FcγRII, and FcγRIII) was suppressed by LPS. Furthermore, suppression was not limited to Fc receptor‐mediated phagocytosis because binding and uptake of C3bi‐opsonized SRBCs to CR3 receptors was also decreased following LPS treatment. LPS did not exert its effects via the production of interleukin‐1 (IL‐1), IL‐6, tumor necrosis factor a, or interferon a/β, because antibodies to these cytokines did not abrogate the effect. The ability of LPS to suppress binding and phagocytosis of microorganisms may contribute to the toxic effects of LPS during gram‐negative sepsis by preventing or delaying elimination of bacteria by host macrophages.