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Moraxella catarrhalis induces ERK- and NF-B-dependent COX-2 and prostaglandin E₂ in lung epithelium

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

CORRESPONDENCE: H. Slevogt, Dept of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité-Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. Fax: 49 30450553906. E-mail: hortense.slevogt{at}charite.de

Keywords: Cyclooxygenase 2, extracellular signal-regulated kinase 1/2, Moraxella catarrhalis, nuclear factor-B, prostaglandin E₂, ubiquitous cell surface protein A1

Received: January 23, 2007
Accepted May 10, 2007

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-B, 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-B 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.

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