Summersgill J T, Molestina R E, Miller R D, Ramirez J A
Division of Infectious Diseases, Dept. of Medicine, University of Louisville School of Medicine, Louisville, KY 40292, USA.
J Infect Dis. 2000 Jun;181 Suppl 3:S479-82. doi: 10.1086/315620.
In order to fulfill the "biological plausibility" criterion of a role for infection with Chlamydia pneumoniae in the pathogenesis of human atherosclerosis, detailed studies on the interaction of this organism with the cell types involved are necessary. This article summarizes the current knowledge on the interaction of C. pneumoniae with human endothelial cells. In vitro, C. pneumoniae can infect human endothelial cells and induce the expression of many molecules that are important mediators of atherogenesis including cytokines, adhesion molecules, chemokines, and molecules with procoagulant activity.
为了满足肺炎衣原体感染在人类动脉粥样硬化发病机制中作用的“生物学合理性”标准，有必要对该病原体与相关细胞类型之间的相互作用进行详细研究。本文总结了目前关于肺炎衣原体与人类内皮细胞相互作用的知识。在体外，肺炎衣原体可感染人类内皮细胞，并诱导许多在动脉粥样硬化发生过程中起重要介导作用的分子表达，包括细胞因子、黏附分子、趋化因子以及具有促凝活性的分子。
