Monocyte-endothelial cell coculture enhances infection of endothelial cells with Chlamydia pneumoniae

To determine the mechanism(s) by which Chlamydia pneumoniae homes to and es tablishes persistent infection in atheromatous lesions, the effect of the i nteraction of monocytes/mcarophages (U937 cells) with human umbilical vein endothelial cells (HUVECs) and transformed human arterial endothelial cells (HMEC-1s) on the susceptibility of endothelial cells to infection with C. pneumoniae was investigated. Infection was enhanced 4.7-fold (HUVECs) and 4 .4-fold (HMEC-1s) after coculture at monocyte-to-endothelial cell ratios of 5 and 2.5, respectively. U937 cells also directly transmitted infection to the endothelial cells, and addition of U937 cell-conditioned media dose-de pendently enhanced the infectivity 2.0- to 2.5-fold. The stimulation of inf ectivity was specific to endothelial cells, because coculturing of monocyte s with epithelial cells did not enhance the susceptibility of epithelial ce lls to infection. The susceptibility of endothelial cells to infection with C. trachomatis and C. psittaci was not enhanced by the monocyte-derived fa ctor(s).