Moraxella catarrhalisinduces ERK- and NF-κB-dependent COX-2 and prostaglandin E2in lung epithelium

Abstract

Moraxella catarrhalisis 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 thatM. catarrhalisinduces COX-2-dependent PGE₂production in pulmonary epithelial cells.In the present study, the authors demonstrate thatM. catarrhalisspecifically induces COX-2 expression and subsequent PGE₂release in pulmonary epithelial cells. Furthermore, the prostanoid receptor subtypes EP2 and EP4 were also upregulated in these cells.TheM. catarrhalis-specific ubiquitous cell surface protein A1 was important for the induction of COX-2 and PGE₂. Moreover,M. catarrhalis-induced COX-2 and PGE₂expression 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 ofMoraxella catarrhalis, extracellular signal-regulated kinase 1/2 and nuclear factor-κB control cyclooxygenase-2 expression and subsequent prostaglandin E₂release by lung epithelial cells.Moraxella catarrhalis-induced prostaglandin E₂expression might counteract lung inflammation promoting colonisation of the respiratory tract in chronic obstructive pulmonary disease patients.