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Infection and Immunity, November 2004, p. 6615-6621, Vol. 72, No. 11
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.11.6615-6621.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Differences in Cell Activation by Chlamydophila pneumoniae and Chlamydia trachomatis Infection in Human Endothelial Cells

Department of Internal Medicine/Infectious Diseases, Charité, University Medicine Berlin, Berlin,¹ Institute of Medical Microbiology and Hygiene, University of Lübeck, Lübeck,² Institute of Moleculare Medicine, Heinrich-Heine University Düsseldorf, Düsseldorf,³ Division of Rheumatology, Department of Medicine, Hannover Medical School, Hanover Germany⁴

Received 8 March 2004/ Returned for modification 3 May 2004/ Accepted 14 July 2004

Seroepidemiological studies and demonstration of viable bacteria in atherosclerotic plaques have linked Chlamydophila pneumoniae infection to the development of chronic vascular lesions and coronary heart disease. In this study, we characterized C. pneumoniae-mediated effects on human endothelial cells and demonstrated enhanced phosphorylation and activation of the endothelial mitogen-activated protein kinase (MAPK) family members extracellular receptor kinase (ERK1/2), p38-MAPK, and c-Jun-NH₂ kinase (JNK). Subsequent interleukin-8 (IL-8) expression was dependent on p38-MAPK and ERK1/2 activation as demonstrated by preincubation of endothelial cells with specific inhibitors for the p38-MAPK (SB202190) or ERK (U0126) pathway. Inhibition of either MAPK had almost no effect on intercellular cell adhesion molecule 1 (ICAM-1) expression. While Chlamydia trachomatis was also able to infect endothelial cells, it did not induce the expression of endothelial IL-8 or ICAM-1. These effects were specific for a direct stimulation with viable C. pneumoniae and independent of paracrine release of endothelial cell-derived mediators like platelet-activating factor, NO, prostaglandins, or leukotrienes. Thus, C. pneumoniae triggers an early signal transduction cascade in target cells that could lead to endothelial cell activation, inflammation, and thrombosis, which in turn may result in or promote atherosclerosis.

Editor: S. H. E. Kaufmann

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