title: Chlamydophila pneumoniae infection of human aortic endothelial cells induces the expression of FC gamma receptor II (FcgammaRII).
abstract: Chronic endothelial infection is believed to be one of the factors able to cause endothelial cell damage and trigger the onset of human atherosclerosis. Chlamydophila pneumoniae infects endothelial cells and has received special attention because of both epidemiological and experimental evidence supporting its role as a risk factor for atherosclerosis. It is also possible that otherwise independent risk factors for atherosclerosis may have synergistic effects. Immune phenomena, such as the formation of circulating immune complexes (IC) containing modified LDL and corresponding antibodies, have been linked to the development of coronary artery disease. The antibodies involved in the immune response to modified lipoproteins are predominantly of the pro-inflammatory IgG1 and IgG3 subclasses. However, it is difficult to understand how circulating IC could cause endothelial damage and initiate the atherosclerotic process, unless they were formed in the subendothelial space or immobilized by endothelial cells. The last hypothesis would be possible if endothelial cells expressed Fcgamma receptors. Healthy endothelial cells do not express Fcgamma receptors, but endothelial cells infected by a variety of infectious agents do. Thus we decided to investigate whether infection of endothelial cells with C. pneumoniae is also able to cause the expression of Fcgamma receptors. The expression of Fcgamma receptors (CD64, 32, and 16) on human aortic endothelial cells infected with C. pneumoniae for 4, 24, 36, and 48 h was studied by flow cytometry. Twenty-four hours after infection 30-40% of the endothelial cells had detectable inclusion bodies, 8-9% of the total number of cells (approximately 25% of the infected cells) expressed FcgammaRII, and about 1.5-2% (5% of infected cells) expressed FcgammaRI and FcgammaRIII. Double-staining studies confirmed that the expression of FcgammaRII was limited to C. pneumoniae-infected endothelial cells. We conclude that C. pneumoniae infection induces primarily the expression of FcgammaRII by endothelial cells and this may be a significant link between two proposed pathogenic mechanisms involved in the pathogenesis of human atherosclerosis.
authors.affiliation: Department of Medicine, Medical University of South Carolina, and Ralph H. Johnson VA Medical Center, Charleston, South Carolina 29425, USA.
authors.forename: Silvana
authors.initials: S
authors.lastname: Vielma
authors.forename: Gabriel
authors.initials: G
authors.lastname: Virella
authors.forename: Adam
authors.initials: A
authors.lastname: Gorod
authors.forename: Maria
authors.initials: M
authors.lastname: Lopes-Virella
mesh_terms: D000936:Antigen-Antibody Complex / Q000378:metabolism; D001011:Aorta / Q000166:cytology / Q000276:immunology / Q000382:microbiology; D001161:Arteriosclerosis / Q000209:etiology*; D002478:Cells, Cultured; D016993:Chlamydophila pneumoniae / Q000472:pathogenicity*; D004730:Endothelium, Vascular / Q000166:cytology / Q000276:immunology / Q000382:microbiology*; D005434:Flow Cytometry; D006801:Humans; D017452:Receptors, IgG / Q000032:analysis / Q000096:biosynthesis*
chemical_list: D000936:Antigen-Antibody Complex; D017452:Receptors, IgG