Kalayoglu M V, Hoerneman B, LaVerda D, Morrison S G, Morrison R P, Byrne G I
Department of Medical Microbiology and Immunology, Universityof Wisconsin Medical School, Madison WI 53706, USA.
J Infect Dis. 1999 Sep;180(3):780-90. doi: 10.1086/314931.
A spectrum of clinical and epidemiologic studies implicate infectious agents, including Chlamydia pneumoniae, in the pathogenesis of atherosclerosis. The complexity of atherosclerotic disease necessitates examining the role of infection in the context of defined risk factors, such as high levels of native low-density lipoprotein (LDL). Although native LDL does not have atherogenic properties, cellular oxidation of LDL alters the lipoprotein into a highly atherogenic form. In this report, C. pneumoniae and chlamydial hsp60, an inflammatory antigen that was recently localized to atheromas, were found to induce cellular oxidation of LDL. These data provide initial evidence that an infectious agent can render LDL atherogenic and suggest a mechanism whereby C. pneumoniae may promote atheroma development.
一系列临床和流行病学研究表明，包括肺炎衣原体在内的感染因子与动脉粥样硬化的发病机制有关。动脉粥样硬化疾病的复杂性使得有必要在特定风险因素（如高水平的天然低密度脂蛋白（LDL））的背景下研究感染的作用。虽然天然LDL不具有致动脉粥样硬化的特性，但LDL的细胞氧化会将脂蛋白转变为高度致动脉粥样硬化的形式。在本报告中，发现肺炎衣原体和衣原体热休克蛋白60（一种最近定位于动脉粥样硬化斑块的炎性抗原）可诱导LDL的细胞氧化。这些数据提供了初步证据，证明感染因子可使LDL具有致动脉粥样硬化性，并提示了肺炎衣原体可能促进动脉粥样硬化斑块发展的机制。
