Campbell Lee Ann, Rosenfeld Michael E
Department of Epidemiology, School of Public Health, Seattle, Washington, USA.
Departments of Environmental, Health and Occupational Sciences and Pathology, University of Washington, Seattle, Washington, USA.
Arch Med Res. 2015 Jul;46(5):339-50. doi: 10.1016/j.arcmed.2015.05.006. Epub 2015 May 21.
Atherosclerosis is a chronic disease hallmarked by chronic inflammation, endothelial dysfunction and lipid accumulation in the vasculature. Although lipid modification and deposition are thought to be a major source of the continuous inflammatory stimulus, a large body of evidence suggests that infectious agents may contribute to atherosclerotic processes. This could occur by either direct effects through infection of vascular cells and/or through indirect effects by induction of cytokine and acute phase reactant proteins by infection at other sites. Multiple bacterial and viral pathogens have been associated with atherosclerosis by seroepidemiological studies, identification of the infectious agent in human atherosclerotic tissue, and experimental studies demonstrating an acceleration of atherosclerosis following infection in animal models of atherosclerosis. This review will focus on those infectious agents for which biological plausibility has been demonstrated in animal models and on the challenges of proving a role of infection in human atherosclerotic disease.
动脉粥样硬化是一种以慢性炎症、内皮功能障碍和血管系统脂质积聚为特征的慢性疾病。尽管脂质修饰和沉积被认为是持续炎症刺激的主要来源，但大量证据表明，感染因子可能促成动脉粥样硬化进程。这可能通过感染血管细胞的直接作用和/或通过其他部位感染诱导细胞因子和急性期反应蛋白的间接作用而发生。血清流行病学研究、在人类动脉粥样硬化组织中鉴定感染因子以及在动脉粥样硬化动物模型中感染后证明动脉粥样硬化加速的实验研究，已将多种细菌和病毒病原体与动脉粥样硬化联系起来。本综述将聚焦于那些在动物模型中已证明具有生物学合理性的感染因子，以及证明感染在人类动脉粥样硬化疾病中的作用所面临的挑战。
