title: Differential expression of the C5a receptor and complement receptors 1 and 3 after LPS stimulation of neutrophils and monocytes.
abstract: Animal experiments recently suggested that administration of anti-C5a, anti-C5a receptor or soluble complement receptor type-1 may be of value in the treatment of septic shock. Because results regarding C5a receptor expression (C5a-R, CD-88) have been found to differ between septic animals and patients, the aim of this study was to investigate the neutrophil and monocyte receptor expression of CD-88 and complement receptor-1 (CR-1, CD-35) after stimulation with lipopolysaccharide (LPS) ex vivo. Whole blood or isolated neutrophils and monocytes from healthy people were incubated with LPS in a dose range of 0.1-1000 ng/ml. The expressions of CD-88 and CD-35 were analysed by means of flow cytometry. For comparison, the expressions of complement receptor-3 (CR-3, CD-11b/CD-18), Fc-gamma receptor type-I (CD-64) and CEACAM-8 (CD-66b) were also investigated. In whole blood, CD-88 expression on neutrophils was reduced (P < 0.05). The expressions of CD-35 and CD-11b were increased both on neutrophils (P < 0.001; P < 0.05) and on monocytes (P < 0.001; P < 0.001). No effect was observed on isolated cells. In agreement with the findings in septic patients, LPS reduced the neutrophil C5a-R expression, whereas the expressions of CR-1 and CR-3 were increased. The effects of LPS were indirect and were mediated via factors in the blood. The clinical significance of this is not known, but may be associated with decreased chemotaxis.
authors.affiliation: Sections of Infectious Diseases, Department of Medical Sciences, Uppsala University, Uppsala, Sweden. mia.furebring@medsci.uu.se
authors.forename: M
authors.initials: M
authors.lastname: Furebring
authors.forename: L
authors.initials: L
authors.lastname: Håkansson
authors.forename: P
authors.initials: P
authors.lastname: Venge
authors.forename: J
authors.initials: J
authors.lastname: Sjölin
mesh_terms: D000328:Adult; D000951:Antigens, Neoplasm / Q000276:immunology; D039481:CD11b Antigen / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000276:immunology; D006801:Humans; D008070:Lipopolysaccharides / Q000276:immunology*; D008565:Membrane Proteins / Q000235:genetics* / Q000276:immunology* / Q000378:metabolism; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology*; D044087:Receptor, Anaphylatoxin C5a; D011951:Receptors, Complement / Q000235:genetics* / Q000276:immunology* / Q000378:metabolism; D017463:Receptors, Complement 3b / Q000235:genetics / Q000276:immunology / Q000378:metabolism
chemical_list: D000951:Antigens, Neoplasm; C488033:C5AR1 protein, human; D039481:CD11b Antigen; D015815:Cell Adhesion Molecules; D008070:Lipopolysaccharides; D008565:Membrane Proteins; D044087:Receptor, Anaphylatoxin C5a; D011951:Receptors, Complement; D017463:Receptors, Complement 3b