Arachidonic acid metabolites in otitis media pathogenesis

Arachidonic acid (AA), which is derived from phospholipids of cell membrane, is metabolized enzymatically into two pathways, one trough cyclooxygenase and the other trough lipoxygenase. Cyclooxygenase products include different prostaglandins (PGs) and thromboxane (Tx), and lipoxygenase products include hydroxyeicosatetraenoic acids (HETEs) and leukotrienes (LTs). Corticosteroids inhibit release of AA, and nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit the activity of cyclooxygenase. Among the various inflammatory mediators of otitis media, AA metabolites - both PGs and LTs - appear to play a major role in the pathogenesis of otitis media. This paper will review studies on AA metabolites in the pathogenesis otitis media. These studies include assays of AA metabolites (eicosanoids) in the middle ear effusions (MEEs) and middle ear tissues, identification of AA metabolites in otitis media, localization of cyclooxygenase in the middle ear mucosa (MEM), effects of exogenous PG on the composition of MEE, and therapeutic uses of inhibitors of AA metabolism.