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Media type:
E-Article
Title:
Signal Transduction Pathways Activated in Endothelial Cells Following Infection with Chlamydia pneumoniae
Contributor:
Krüll, Matthias;
Klucken, Andrea C.;
Wuppermann, Frederik N.;
Fuhrmann, Oliver;
Magerl, Christian;
Seybold, Joachim;
Hippenstiel, Stefan;
Hegemann, Johannes H.;
Jantos, Christian A.;
Suttorp, Norbert
imprint:
The American Association of Immunologists, 1999
Published in:The Journal of Immunology
Language:
English
DOI:
10.4049/jimmunol.162.8.4834
ISSN:
0022-1767;
1550-6606
Origination:
Footnote:
Description:
<jats:title>Abstract</jats:title>
<jats:p>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 (β1 and β2 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-κB 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.</jats:p>