Infection and Atherosclerosis Development.

Infection and Atherosclerosis Development.
复制标题

DOI:
10.1016/j.arcmed.2015.05.006
复制
发表时间:
2015-07
影响因子:
7.7
通讯作者:
Rosenfeld ME
Rosenfeld ME
中科院分区:
医学4区
文献类型:
--
作者:
Campbell LA;Rosenfeld ME

文献摘要

被引文献

相似文献

动脉粥样硬化是一种慢性疾病,以慢性炎症、内皮功能障碍和血管系统中的脂质堆积为特征。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,感染性因素可能在动脉粥样硬化过程中起作用。这可以通过感染血管细胞的直接作用和/或通过在其他部位感染诱导细胞因子和急性时相反应蛋白的间接作用而发生。血清流行病学研究、人类动脉粥样硬化组织中感染性病原体的鉴定以及在动脉粥样硬化动物模型中感染后动脉粥样硬化加速的实验研究表明,多种细菌和病毒病原体与动脉粥样硬化有关。这篇综述将集中于那些在动物模型中已证明生物学可信的感染性病原体,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。
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.