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*
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 1015 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.
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