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Signal Transduction Pathways Activated in Endothelial Cells Following Infection with Chlamydia pneumoniae¹

Matthias Krüll^*, Andrea C. Klucken^*, Frederik N. Wuppermann, Oliver Fuhrmann^*, Christian Magerl^*, Joachim Seybold^*, Stefan Hippenstiel^*, Johannes H. Hegemann, Christian A. Jantos and Norbert Suttorp^2,§

^* Department of Internal Medicine, Justus-Liebig-University, Giessen, Germany; Institute of Medical Microbiology, Justus-Liebig-University, Giessen, Germany; Institute of Microbiology, Heinrich-Heine-University, Düsseldorf, Germany; and ^§ Charite, Department of Internal Medicine, Humboldt-University, Berlin, Germany

Chlamydia pneumoniae is an important respiratory pathogen. Recently, its presence has been demonstrated in atherosclerotic lesions. In this study, we characterized C. pneumoniae-mediated activation of endothelial cells and demonstrated an enhanced expression of endothelial adhesion molecules followed by subsequent rolling, adhesion, and transmigration of leukocytes (monocytes, granulocytes). These effects were blocked by mAbs against endothelial and/or leukocyte adhesion molecules (ß₁ and ß₂ integrins). Additionally, activation of different signal transduction pathways in C. pneumoniae-infected endothelial cells was shown: protein tyrosine phosphorylation, up-regulation of phosphorylated p42/p44 mitogen-activated protein kinase, and NF-B activation/translocation occurred within 10–15 min. Increased mRNA and surface expression of E-selectin, ICAM-1, and VCAM-1 were noted within hours. Thus, C. pneumoniae triggers a cascade of events that could lead to endothelial activation, inflammation, and thrombosis, which in turn may result in or may promote atherosclerosis.