Interactions of Chlamydia pneumoniae with human endothelial cells.

Abstract

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.