Expression of adhesion molecules on endothelial cells stimulated by Chlamydia pneumoniae.
Previous studies have shown that C. pneumoniae is able to infect human endothelial cells in vitro. In this report, the ability of C. pneumoniae to 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. pneumoniae was 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. pneumoniae to grow in endothelial cells and to stimulate the expression of adhesion molecules essential for leukocyte-endothelial cell interactions suggests a role for C. pneumoniae as a local pathogenetic factor in vascular inflammatory alterations, including atherogenesis.
Kaukoranta-Tolvanen
S S
SS
Department of Virology, University of Helsinki, Finland.
Ronni
T
T
Leinonen
M
M
Saikku
P
P
Laitinen
K
K
D002478:Cells, Cultured; D016993:Chlamydophila pneumoniae / Q000276:immunology*; D019040:E-Selectin / Q000276:immunology*; D004730:Endothelium, Vascular / Q000166:cytology / Q000276:immunology*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000276:immunology*; D014471:Umbilical Veins / Q000166:cytology / Q000276:immunology; D019010:Vascular Cell Adhesion Molecule-1 / Q000276:immunology*
D019040:E-Selectin; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1