Kalayoglu M V, Morrison R P, Morrison S G, Yuan Y, Byrne G I
Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, Madison, WI 53706, USA. gibyrne@facstaff. wisc.edu
J Infect Dis. 2000 Jun;181 Suppl 3:S483-9. 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.
一系列流行病学、病理学及动物模型研究的数据表明，肺炎衣原体感染与冠状动脉疾病相关，但尚不清楚该病原体如何引发或促进动脉粥样硬化。据推测，肺炎衣原体通过特定毒力决定因素引发关键的致动脉粥样硬化事件。肺炎衣原体通过衣原体脂多糖（cLPS）诱导单核吞噬细胞泡沫细胞形成，并通过衣原体热休克蛋白60（chsp60）诱导低密度脂蛋白氧化。因此，不同的衣原体成分可能促进动脉粥样硬化发展过程中涉及的不同事件。本文讨论了涉及cLPS和chsp60在动脉粥样硬化发病机制中的数据，并提出了新方法，试图阐明这些假定的毒力决定因素如何向单核吞噬细胞发出信号，以调节脂蛋白流入和修饰。
