RT Journal Article SR Electronic T1 Moraxella catarrhalis induces ERK- and NF-κB-dependent COX-2 and prostaglandin E2 in lung epithelium JF European Respiratory Journal JO Eur Respir J FD European Respiratory Society SP 443 OP 451 DO 10.1183/09031936.00008707 VO 30 IS 3 A1 P. D. N'Guessan A1 B. Temmesfeld-Wollbrück A1 J. Zahlten A1 J. Eitel A1 S. Zabel A1 B. Schmeck A1 B. Opitz A1 S. Hippenstiel A1 N. Suttorp A1 H. Slevogt YR 2007 UL http://erj.ersjournals.com/content/30/3/443.abstract AB Moraxella catarrhalis is a major cause of infectious exacerbations of chronic obstructive lung disease. Cyclooxygenase (COX)-derived prostaglandins, such as prostaglandin E2 (PGE2), are considered to be important regulators of lung function. The present authors tested the hypothesis that M. catarrhalis induces COX-2-dependent PGE2 production in pulmonary epithelial cells. In the present study, the authors demonstrate that M. catarrhalis specifically induces COX-2 expression and subsequent PGE2 release in pulmonary epithelial cells. Furthermore, the prostanoid receptor subtypes EP2 and EP4 were also upregulated in these cells. The M. catarrhalis-specific ubiquitous cell surface protein A1 was important for the induction of COX-2 and PGE2. Moreover, M. catarrhalis-induced COX-2 and PGE2 expression was dependent on extracellular signal-regulated kinase 1/2-driven activation of nuclear factor-κB, but not on the activation of p38 mitogen-activated protein kinase. In conclusion, the present data suggest that ubiquitous cell surface protein A1 of Moraxella catarrhalis, extracellular signal-regulated kinase 1/2 and nuclear factor-κB control cyclooxygenase-2 expression and subsequent prostaglandin E2 release by lung epithelial cells. Moraxella catarrhalis-induced prostaglandin E2 expression might counteract lung inflammation promoting colonisation of the respiratory tract in chronic obstructive pulmonary disease patients.