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

被引:73
作者
Kalayoglu, MV
Indrawati
Morrison, RP
Morrison, SG
Yuan, Y
Byrne, GI
机构
[1] Univ Wisconsin, Sch Med, Dept Med Microbiol & Immunol, Madison, WI 53706 USA
[2] Montana State Univ, Dept Microbiol, Bozeman, MT 59717 USA
[3] Pathogenesis Corp, Seattle, WA USA
关键词
D O I
10.1086/315619
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:S483 / S489
页数:7
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