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Published ahead of print on December 9, 2005, doi:10.1165/rcmb.2004-0157OC

Am. J. Respir. Cell Mol. Biol., Volume 34, Number 3, March 2006, 375-382

A more recent version of this article appeared on March 1, 2006
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Submitted on May 10, 2004
Revised on December 5, 2005

Mechanisms of Chlamydophila pneumoniae Mediated GM-CSF Release in Human Bronchial Epithelial Cells

Matthias Krull1*, Petra Bockstaller1, Frederik N Wuppermann2, Andrea C Klucken1, Jorg Muhling3, Bernd Schmeck1, Joachim Seybold1, Clemens Walter1, Matthias Maass4, Simone Rosseau1, Johannes H Hegemann2, Norbert Suttorp1, and Stefan Hippenstiel1

1 Department of Internal Medicine/Infectious Diseases, Charite, Universitatsmedizin, Berlin, Germany, 2 Institute of Microbiology, Heinrich-Heine University, Dusseldorf, Germany, 3 Department of Anaesthesiology, Intensive Care Medicine, and Pain Therapy, Justus-Liebig-University, Giessen, Germany, 4 SALK Labor, Salzburger Landeskliniken, Salzburg, Austria

* To whom correspondence should be addressed. E-mail: matthias.kruell{at}charite.de.

Chlamydophila pneumoniae is an important respiratory pathogen. In this study we characterized C. pneumoniae strain TW183-mediated activation of human small airway epithelial cells (SAEC) and the bronchial epithelial cell line BEAS-2B and demonstrated time-dependent secretion of granulocyte macrophage colony-stimulating factor (GM-CSF) upon stimulation. TW183 activated p38 mitogen activated protein kinase (MAPK) in epithelial cells. Kinase inhibition by SB202190 blocked chlamydia mediated GM-CSF release on mRNA- and protein-level. In addition, the chemical inhibitor as well as dominant negative mutants of p38 MAPK isoforms p38{alpha}, {beta}2, and {gamma} inhibited C. pneumoniae-related NF-{kappa}B activation. In contrast, blocking of MAPK ERK, c-Jun kinase/JNK or PI-3 Kinase showed no effect on Chlamydia related epithelial cell GM-CSF release. UV-inactivated pathogens as compared to viable bacteria induced a smaller GM-CSF -release suggesting that viable Chlamydia were only partly required for a full effect. Presence of an anti-chlamydial outer membrane protein-A (Omp-A) antibody reduced and addition of recombinant heat-shock protein 60 from C. pneumoniae (cHsp60, GroEL-1) enhanced GM-CSF -release suggesting a role of these proteins in epithelial cell activation. Our data demonstrate that C. pneumoniae triggers an early proinflammatory signaling cascade involving p38 MAPK dependent NF-{kappa}B activation resulting in subsequent GM-CSF release. C. pneumoniae-induced epithelial cytokine liberation may contribute significantly to inflammatory airway diseases like chronic obstructive pulmonary disease (COPD) or bronchial asthma.




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