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A more recent version of this article appeared on May 1, 2004

Papers In Press, published online ahead of print February 16, 2004
J. Lipid Res., doi:10.1194/jlr.M300456-JLR200
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Submitted on October 31, 2003
Revised on December 23, 2003
Accepted on February 6, 2004

Oxidized LDL further enhances expression of adhesion molecules in Chlamydophila pneumoniae-infected endothelial cells

Silvana A. Vielma, Marina Mironova, Ja-Ran Ku, and Maria F. Lopes-Virella

Department of Medicine, Medical University of South Carolina, Charleston, SC 29425

Corresponding Author: virellam{at}musc.edu

Chlamydophila pneumoniae is a common respiratory pathogen that has been shown to be associated with coronary artery disease. Recent studies have shown that one of the possible mechanisms explaining the atherogenicity of C. pneumoniae is overexpression of cell-adhesion molecules (CAM) in infected endothelial cells. We investigated whether exposure of C. pneumoniae- infected endothelial cells to oxidize LDL (oxLDL) leads to further up-regulation of CAMs. Flow cytometry and immunoblot analysis of human aortic endothelial cells (HAEC) was performed for intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin. ICAM-1 was expressed in 78.7% of C. pneumoniae –infected HAEC. The addition of oxLDL (100mg/ml) to infected HAEC increased the proportion of ICAM-1 positive cells to 92%. VCAM-1 was only observed in 9.3% of infected HAEC, however addition of oxLDL had no further effect on the surface expression of VCAM-1. C. pneumoniae also upregulated the surface expression of E-selectin on 52.2% of the cells and incubation with oxLDL further increased the proportion of positive cells to 63.64%. In conclusion, C. pneumoniae upregulated the expression of adhesion molecules ICAM-1, VCAM-1 and E-selectin on HAEC. Addition of oxLDL to the infected cells further enhanced the surface expression of ICAM-1 and E-selectin.


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