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- W2004705655 abstract "Previous studies have shown thatC. pneumoniaeis able to infect human endothelial cellsin vitro. In this report, the ability ofC. pneumoniaeto 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. pneumoniaewas 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 ofC. pneumoniaeto grow in endothelial cells and to stimulate the expression of adhesion molecules essential for leukocyte–endothelial cell interactions suggests a role forC. pneumoniaeas a local pathogenetic factor in vascular inflammatory alterations, including atherogenesis." @default.
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- W2004705655 date "1996-11-01" @default.
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- W2004705655 title "Expression of adhesion molecules on endothelial cells stimulated byChlamydia pneumoniae" @default.
- W2004705655 doi "https://doi.org/10.1006/mpat.1996.0071" @default.
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