Expression of adhesion molecules on endothelial cells stimulated by Chlamydia pneumoniae

Microb Pathog. 1996 Nov;21(5):407-11. doi: 10.1006/mpat.1996.0071.

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.

MeSH terms

  • Cells, Cultured
  • Chlamydophila pneumoniae / immunology*
  • E-Selectin / immunology*
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / immunology*
  • Humans
  • Intercellular Adhesion Molecule-1 / immunology*
  • Umbilical Veins / cytology
  • Umbilical Veins / immunology
  • Vascular Cell Adhesion Molecule-1 / immunology*

Substances

  • E-Selectin
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1