title: Expression of adhesion molecules on endothelial cells stimulated by Chlamydia pneumoniae.
abstract: 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.
authors.affiliation: Department of Virology, University of Helsinki, Finland.
authors.forename: S S
authors.initials: SS
authors.lastname: Kaukoranta-Tolvanen
authors.forename: T
authors.initials: T
authors.lastname: Ronni
authors.forename: M
authors.initials: M
authors.lastname: Leinonen
authors.forename: P
authors.initials: P
authors.lastname: Saikku
authors.forename: K
authors.initials: K
authors.lastname: Laitinen
mesh_terms: 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*
chemical_list: D019040:E-Selectin; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1