Expression of adhesion molecules on endothelial cells stimulated by Chlamydia pneumoniae

Abstract

Previous studies have shown that C. pneumoniaeis able to infect human endothelial cells in vitro. In this report, the ability of C. pneumoniaeto induce the expression of E-selectin or endothelial-leukocyte adhesion molecule 1 (ELAM-1), intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) on human umbilical vein endothelial (HUVE) cell surface was investigated. C. pneumoniaewas found to cause a moderate upregulation of the adhesion molecules. Maximal expression of E-selectin was noted at 6 h post infection (p.i.) and that of ICAM-1 and VCAM-1 at 20 h p.i. The capability of C. pneumoniaeto grow in endothelial cells and to stimulate the expression of adhesion molecules essential for leukocyte–endothelial cell interactions suggests a role for C. pneumoniaeas a local pathogenetic factor in vascular inflammatory alterations, including atherogenesis.