Chlamydial Virulence Determinants in Atherogenesis: The Role of Chlamydial Lipopolysaccharide and Heat Shock Protein 60 in Macrophage-Lipoprotein Interactions

• Published in: The Journal of infectious diseases Vol. 181; no. Supplement-3; pp. S483 - S489
• Main Authors: Kalayoglu, Murat V., Indrawati, Morrison, Richard P., Morrison, Sandra G., Yuan, Ying, Byrne, Gerald I.
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Chicago, IL The University of Chicago Press 01.06.2000; University of Chicago Press
• Subjects: Animals; Arteriosclerosis - etiology; Arteriosclerosis - microbiology; Arteriosclerosis - physiopathology; Atherosclerosis; Atherosclerosis (general aspects, experimental research); Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Chaperonin 60 - metabolism; Chlamydia Infections - microbiology; Chlamydia pneumoniae; Chlamydia pneumoniae Infection and Lipid Metabolism; Chlamydophila pneumoniae - pathogenicity; Cholesterols; Foam cells; Humans; Infections; Lipids; Lipopolysaccharides - metabolism; Lipoproteins; Lipoproteins - metabolism; Macrophages; Macrophages - metabolism; Medical sciences; Monocytes; Oxidation; Oxidation-Reduction; Phagocytes; Virulence; Chlamydia pneumoniae; Chlamydiaceae; Pathogenesis; Virulence; Cardiovascular disease; Review; Lipoprotein; Infection; Vascular disease; Atherosclerosis; Heat shock protein; Bacteriosis; Chlamydiales; Lipopolysaccharide; Bacteria; Chlamydiosis; Macrophage
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1086/315619

Data from a spectrum of epidemiologic, pathologic, and animal model studies show that Chlamydia pneumoniae infection is associated with coronary artery disease, but it is not clear how the organism may initiate or promote atherosclerosis. It is postulated that C. pneumoniae triggers key atherogenic events through specific virulence determinants. C. pneumoniae induces mononuclear phagocyte foam cell formation by chlamydial lipopolysaccharide (cLPS) and low-density lipoprotein oxidation by chlamydial hsp60 (chsp60). Thus, different chlamydial components may promote distinct events implicated in the development of atherosclerosis. Data implicating cLPS and chsp60 in the pathogenesis of atherosclerosis are discussed and novel approaches are presented for attempting to elucidate how these putative virulence determinants signal mononuclear phagocytes to modulate lipoprotein influx and modification.