Chlamydial virulence determinants in atherogenesis: The role of chlamydiallipopolysaccharide and heat shock protein 60 in macrophage-lipoprotein interactions

Data from a spectrum of epidemiologic, pathologic, and animal model studies show that Chlamydia pneumoniae infection is associated with coronary arter y disease, but it is not clear how the organism may initiate or promote ath erosclerosis. It is postulated that C. pneumoniae triggers key atherogenic events through specific virulence determinants. C. pneumoniae induces monon uclear 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 pre sented for attempting to elucidate how these putative virulence determinant s signal mononuclear phagocytes to modulate lipoprotein influx and modifica tion.