Bacterial endotoxin selectively prevents the expression of scavenger- receptor activity on human monocyte-macrophages

• Published in: The Journal of immunology (1950) Vol. 134; no. 6; pp. 3718 - 3721
• Main Authors: Van Lenten, BJ, Fogelman, AM, Seager, J, Ribi, E, Haberland, ME, Edwards, PA
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 01.06.1985; American Association of Immunologists
• Subjects: Apolipoproteins E - biosynthesis; Applied sciences; Cytotoxicity, Immunologic - drug effects; Endocytosis - drug effects; Endotoxins - pharmacology; Exact sciences and technology; Humans; Immunosuppressive Agents - pharmacology; Lipopolysaccharides - pharmacology; Macrophage Activation - drug effects; Monocytes - immunology; Monocytes - metabolism; Other techniques and industries; Receptors, Cell Surface - drug effects; Receptors, Lipoprotein
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.134.6.3718

Concentrations of bacterial lipopolysaccharide (LPS) as low as 1 ng/ml suppressed the activity of the scavenger receptor on cultured human monocyte-macrophages. In contrast, concentrations of LPS as high as 100 ng/ml had no effect on the activity of the low density lipoprotein (LDL) receptor. LPS and purified forms of the lipid A moiety of LPS were effective in suppressing scavenger receptor activity. However, acid hydrolysis of the labile phosphate group of the native diphosphorylated lipid A to form monophosphoryl lipid A rendered the molecule ineffective in suppressing scavenger receptor activity. LPS at a concentration of 100 ng/ml had no effect on the secretion of apolipoprotein E, phagocytic activity, tumoricidal activity, or the protein content of monocyte-macrophages. We conclude that the active component of LPS that mediates suppression of scavenger receptor activity is diphosphoryl lipid A.