High concentrations of bacterial lipopolysaccharide, but not microbial infection-induced inflammation, activate macrophage C3 receptors for phagocytosis

• Published in: The Journal of immunology (1950) Vol. 145; no. 2; pp. 697 - 701
• Main Authors: Griffin, FM, Jr, Mullinax, PJ
• Format: Journal Article
• Language: English
• Published: United States Am Assoc Immnol 15.07.1990
• Subjects: Animals; Bacterial Infections - physiopathology; Dose-Response Relationship, Drug; Inflammation - physiopathology; Lipopolysaccharides - administration & dosage; Macrophage Activation - drug effects; Macrophage-1 Antigen; Macrophages - physiology; Membrane Fluidity; Mice; Mice, Inbred Strains; Peritoneal Cavity - cytology; Phagocytosis; Receptors, Complement - physiology; T-Lymphocytes - physiology
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.145.2.697

Macrophage C3 receptors are normally immobilized in the plane of the cells' plasma membrane and are unable to promote phagocytosis even though they promote avid particle binding. We have previously identified a lymphokine that activates macrophage C3 receptors for phagocytosis both in vitro and in vivo, and others have found that certain types of nonimmunologically mediated inflammation are also able to activate mononuclear phagocyte C3 receptors. These findings raised the possibility that macrophage C3 receptor activation is a universal consequence of inflammation. We sought in the present experiments to determine whether or not inflammation induced by microbial infection in a nonimmune host resulted in activation of macrophage C3 receptors. We injected mice i.p. with either viable microorganisms, microbe-containing immune complexes, or bacterial LPS. Macrophages were harvested by peritoneal lavage 4 days later; nearly all lavage fluids grew the microorganism with which the mouse had been injected, indicating that an infection had been established. Monolayers of macrophages were established and their interaction with sheep E coated with C3 (EIgMC) was determined. All macrophages bound EIgMC, but only macrophages from mice injected with either very high concentrations of LPS or microbe-containing immune complexes ingested them. C3 receptors of macrophages that ingested EIgMC were mobile; others were not. Thus, inflammation induced by microbial infection does not commonly, if at all, activate macrophage C3 receptors; microbe-containing immune complexes and high concentrations of LPS do. The mechanism of receptor activation in each case is C3 receptor mobilization, which is probably mediated by a lymphokine.