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This Article Full Text Full Text (PDF) All Versions of this Article: 292/1/L267    most recent 00100.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by N'Guessan, P. D. Articles by Hippenstiel, S. Search for Related Content PubMed PubMed Citation Articles by N'Guessan, P. D. Articles by Hippenstiel, S.

Legionella pneumophila-induced PKC-, MAPK-, and NF-B-dependent COX-2 expression in human lung epithelium

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 IB and activated NF-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 was observed in infected cells. PKC and p38 and p42/44 MAP kinase inhibitors reduced PGE₂ release and COX-2 expression. In summary, PKC 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

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