Rosenfeld M E, Blessing E, Lin T M, Moazed T C, Campbell L A, Kuo C
Department of Pathobiology and Interdisciplinary Graduate Program in Nutritional Sciences, University of Washington, Seattle, WA 98195.
J Infect Dis. 2000 Jun;181 Suppl 3:S492-7. doi: 10.1086/315618.
Atherosclerotic lesions are initiated and progress largely as a result of a chronic, fibroproliferative, inflammatory response. This review discusses how Chlamydia pneumoniae could conceivably contribute to this chronic inflammatory response and reports on recent in vivo and in vitro studies. In vivo studies in mice demonstrate that C. pneumoniae infection is disseminated to the artery wall following infection in the lung by alveolar macrophages. Recent in vitro studies show that infected U937 cells can directly transfer infection to endothelial cells and can indirectly increase the susceptibility of endothelial cells to C. pneumoniae infection. Loading of RAW 264.7 cells with modified forms of low-density lipoprotein increases the resistance of the cells to C. pneumoniae infection and also increases the susceptibility to the combined toxic effects of modified lipids and C. pneumoniae infection.
动脉粥样硬化病变的发生和发展很大程度上是慢性纤维增生性炎症反应的结果。本综述讨论了肺炎衣原体如何可能促成这种慢性炎症反应，并报告了近期的体内和体外研究。小鼠体内研究表明，肺炎衣原体感染通过肺泡巨噬细胞在肺部感染后扩散至动脉壁。近期的体外研究表明，感染的U937细胞可直接将感染传递给内皮细胞，并可间接增加内皮细胞对肺炎衣原体感染的易感性。用修饰形式的低密度脂蛋白加载RAW 264.7细胞可增加细胞对肺炎衣原体感染的抵抗力，同时也增加对修饰脂质和肺炎衣原体感染联合毒性作用的易感性。
