Modulation of the release of 9-hydroxy-octadecadienoic acid and other fatty acid derived mediators from guinea-pig pulmonary macrophages.

Non-stimulated guinea-pig pulmonary macrophages (PM) convert arachidonic acid to thromboxane B2 and 12-hydroxy-heptadecatrienoic acid, whereas linoleic acid is metabolized to two hydroxy compounds, i.e. 9-hydroxy- and 13-hydroxy-octadecadienoic acid. Coincubation of PM with immune serum (2% v/v) resulted in a profound reduction of the release of these products. This effect seemed to be due to an inhibitory action on cyclooxygenase activity. Control serum also possessed inhibitory properties towards the release of fatty acid metabolites, possibly due to an effect on phospholipase activity. Because of the radical scavenging properties of 9-hydroxy-octadecadienoic acid, the modulation of the release of this product may be an important determinant in macrophage function.