dinoprost and Lung-Diseases--Parasitic

The ability of arachidonic acid (AA) metabolites to regulate I-region-associated (Ia) antigen expression on macrophages from schistosome-egg-induced pulmonary granulomas was examined. The prostaglandin (PG) analog 15-S-15-CH3-PGE1 (M-PGE1) and PGF2 alpha were found to modulate the kinetics of Ia expression when administered in vivo. Methyl-PGE1 significantly suppressed Ia antigen expression by hypersensitivity granuloma macrophages, while PGF2 alpha appeared to potentiate the expression. Lymphokine-induced Ia antigen expression by cultured granuloma macrophages was likewise dramatically inhibited by M-PGE1. Further analysis using systemically administered inhibitors of AA metabolism demonstrated that the cyclooxygenase inhibitor indomethacin caused augmentation of Ia expression. In contrast, lipoxygenase inhibitors significantly reduced both Ia expression and granuloma size. The role of AA metabolites in modulating chronic inflammation is discussed.

Topics: Alprostadil; Animals; Arachidonic Acids; Cells, Cultured; Dinoprost; Female; Granuloma; Histocompatibility Antigens Class II; Hypersensitivity; Kinetics; Lung Diseases, Parasitic; Lymphokines; Macrophages; Mice; Mice, Inbred CBA; Prostaglandins E, Synthetic; Prostaglandins F; Schistosoma mansoni; Schistosomiasis