Pulmonary surfactant phosphatidyl glycerol inhibits Mycoplasma pneumoniae stimulated eicosanoid production from human alveolar macrophages and mouse RAW264.7 macrophages

Abstract

Mycoplasma pneumoniae (Mpn) is a common etiologic agent of respiratory infection in children and adults that has been associated with serious exacerbations of asthma. Mpn induces cyclooxygenase‐2 (COX‐2) and the generation of eicosanoids from human alveolar macrophages (ThromboxaneB2, PGD2 and PGF2α) and RAW264.7 cells (PGD2 and PGE2). Inhibition of the phosphorylation of p42/44 MAP kinase, or the activity of cytosolic phospholipase A2α, completely abolished Mpn induced AA release from macrophages. The minor pulmonary surfactant phospholipid palmitoyl‐oleyl ‐phosphatidylglycerol (POPG) antagonized the proinflammatory actions of Mpn by blocking the release of eicosanoids from the cells. The action of POPG reduced the phosphorylation of p42/44 and the expression of COX‐2 induced by Mpn. The effects of POPG were structure dependent and not reproduced by dipalmitoyl‐PG. These data suggest that POPG can play an important role in suppressing pathogen induced inflammation in the lung.