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Am J Physiol Lung Cell Mol Physiol 292: L267-L277, 2007. First published September 29, 2006; doi:10.1152/ajplung.00100.2006
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Legionella pneumophila-induced PKC{alpha}-, MAPK-, and NF-{kappa}B-dependent COX-2 expression in human lung epithelium

Philippe Dje N'Guessan,1 Mirabelle O. Etouem,1 Bernd Schmeck,1 Andreas C. Hocke,1 Stefanie Scharf,1 Kremena Vardarova,1 Bastian Opitz,1 Antje Flieger,2 Norbert Suttorp,1 and Stefan Hippenstiel1

1Department of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité - Universitätsmedizin Berlin; and 2NG5 Pathogenesis of Legionella Infection, Robert Koch-Institut, Berlin, Germany

Submitted 20 March 2006 ; accepted in final form 26 September 2006

Legionella pneumophila causes community- and hospital-acquired pneumonia. Lung airway and alveolar epithelial cells comprise an important barrier against airborne pathogens. Cyclooxygenase (COX) and microsomal PGE2 synthase-1 (mPGES-1)-derived prostaglandins like prostaglandin E2 (PGE2) are considered as important regulators of lung function. Herein we tested the hypothesis that L. pneumophila induced COX-2 and mPGES-1-dependent PGE2 production in pulmonary epithelial cells. Legionella induced the release of PGE2 in primary human small airway epithelial cells and A549 cells. This was accompanied by an increased expression of COX-2 and mPGES-1 as well as an increased PLA2 activity in infected cells. Deletion of the type IV secretion system Dot/Icm did not impair Legionella-related COX-2 expression or PGE2 release in A549 cells. L. pneumophila induced the degradation of I{kappa}B{alpha} and activated NF-{kappa}B. Inhibition of IKK blocked L. pneumophila-induced PGE2 release and COX-2 expression. We noted activation of p38 and p42/44 MAP kinase in Legionella-infected A549 cells. Moreover, membrane translocation and activation of PKC{alpha} was observed in infected cells. PKC{alpha} and p38 and p42/44 MAP kinase inhibitors reduced PGE2 release and COX-2 expression. In summary, PKC{alpha} and p38 and p42/44 MAP kinase controlled COX-2 expression and subsequent PGE2 release by Legionella-infected lung epithelial cells. These pathways may significantly contribute to the host response in Legionnaires' disease.

alveolar epithelium; protein kinase C; prostaglandin E2; cyclooxygenase-2; phospholipase A2; microsomal PGE2 synthase-1; mitogen-activated protein kinase


Address for reprint requests and other correspondence: S. Hippenstiel, Dept. of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany (e-mail: stefan.hippenstiel{at}charite.de)




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