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Published online before print May 30, 2007
Eur Respir J 2007, doi:10.1183/09031936.00008707
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ORIGINAL ARTICLE

Moraxella catarrhalis induces ERK- and NF-{kappa}b-dependent COX-2 and pge2 in lung epithelium

P.D. N'Guessan 1, B. Temmesfeld-Wollbrück 1, J. Zahlten 1, J. Eitel 1, S. Zabel 1, B. Schmeck 1, B. Opitz 1, S. Hippenstiel 1, N. Suttorp 1, H. Slevogt 1*

1 Dept of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité-Universitätsmedizin Berlin, 13353 Berlin, Germany

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


  Abstract

Moraxella catarrhalis is a major cause of infectious exacerbations of chronic obstructive lung disease (COPD). Cyclooxygenase (COX) derived prostaglandins like prostaglandin E2 (PGE2) are considered as important regulators of lung function. Herein we tested the hypothesis that M. catarrhalis induced COX-2-dependent PGE2 production in pulmonary epithelial cells.

In this study we demonstrated that M. catarrhalis specifically induced COX-2 and subsequent PGE2 release in pulmonary epithelial cells. Furthermore, the prostanoid receptors EP2 and EP4 were also up regulated in these cells. The M. catarrhalis-specific ubiquitous cell surface protein A1 (UspA1) was important for the induction of COX-2 and PGE2. Moreover, M. catarrhalis-induced COX-2 and PGE2 expression was dependent on ERK1/2 driven activation of NF-{kappa}B, but not on the activation of p38 MAPK.

In conclusion our data suggests that UspA1 of M. catarrhalis, ERK1/2- and NF-{kappa}B controlled COX-2 expression and subsequent PGE2 release by lung epithelial cells. M. catarrhalis-induced PGE2 expression might counteract lung inflammation promoting colonization of the respiratory tract in COPD-patients.

Keywords:  Cyclooxygenase 2, ERK1/2, Moraxella catarrhalis, NF-{kappa}B, Prostaglandine E2, UspA1




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