Uptake of dihomo-γ-linolenic acid by murine macrophages increases series-1 prostaglandin release following lipopolysaccharide treatment

Administration of dihomo-γ-linolenic acid is useful for atopic dermatitis and atherosclerosis in mice; however, the metabolites of dihomo-γ-linolenic acid have been little studied. We employed a method which enabled simultaneous analysis of nine prostaglandins using liquid chromatography–tandem mass spectrometry, and determined the concentrations of prostaglandins in the supernatants of cultures of mouse peritoneal macrophages stimulated with lipopolysaccharide after pre-incubation with dihomo-γ-linolenic acid, arachidonic acid, or eicosapentaenoic acid. Accumulated prostaglandin concentrations from mouse macrophages with dihomo-γ-linolenic acid uptake increased in a dihomo-γ-linolenic acid concentration-dependent fashion. These increases were mainly due to prostaglandin D1 and prostaglandin E1. The order of accumulated prostaglandin concentrations was dihomo-γ-linolenic acid>arachidonic acid>eicosapentaenoic acid in supernatants with the same concentration of polyunsaturated fatty acid. Since mouse macrophages can clearly produce series-1 prostaglandins, they must be formed in vivo. These findings suggest that the effects of dihomo-γ-linolenic acid on diseases may be due to series-1 prostaglandins.