Abstract

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 of the atherogenicity of C. pneumoniae is overexpression of cell adhesion molecules (CAMs) in infected endothelial cells. We investigated whether exposure of C. pneumoniae-infected endothelial cells to oxidized LDL (oxLDL) leads to further upregulation of CAMs. Flow cytometry and immunoblot analysis of human aortic endothelial cells (HAECs) 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 HAECs. The addition of oxLDL (100 microg/ml) to infected HAECs increased the proportion of ICAM-1-positive cells to 92%. VCAM-1 was only observed in 9.3% of infected HAECs, and the 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 the adhesion molecules ICAM-1, VCAM-1, and E-selectin on HAECs. The addition of oxLDL to the infected cells further enhanced the surface expression of ICAM-1 and E-selectin.

Highlights

  • Chlamydophila pneumoniae is a common respiratory pathogen that has been shown to be associated with coronary artery disease

  • Expression of intracellular adhesion molecule-1 (ICAM-1) in C. pneumoniae-infected human aortic endothelial cells (HAECs) Infection of HAECs by C. pneumoniae led to a timedependent increase in the expression of ICAM-1

  • Our results show that the expression of adhesion molecules in HAECs infected with C. pneumoniae AR39 is enhanced when the cells are incubated in medium containing oxidized LDL (oxLDL)

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Summary

Introduction

Chlamydophila pneumoniae is a common respiratory pathogen that has been shown to be associated with coronary artery disease. The incubation of macrophages with oxLDL results in the release of proinflammatory cytokines such as interleukin-1 and tumor necrosis factor (TNF), which are known to upregulate the expression of cell adhesion molecules (CAMs) [7,8,9,10,11]. Another factor known to cause increased expression of cell adhesion molecules in the endothelium is Chlamydophila pneumoniae infection [12]. The presence of circulating C. pneumoniae-specific immune complexes in a high

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