The inflammatory modulating activity of specific prostaglandins has been examined for both immune and foreign-body types of pulmonary granulomas. Lung granuloma formation generated in mice by embolization of Schistosoma mansoni eggs was markedly suppressed by treatment with the stable, functional analog of prostaglandin E, (PGE1), (15-(S)-15-methyl PGE1) while treatment with PGF2 alpha augmented the granulomatous response. Despite marked effects on egg-induced granuloma formation, PGs had no significant effect on the foreign body lesion induced by Sephadex beads. Likewise, PGs had no effect on the primary antibody response to schistosome egg antigens. However, notable derangements in splenic lymphoid populations occurred. While T-cell numbers appeared constant in face of PG treatment, B-cell populations were depressed by methyl-PGE1 and augmented by PGF2 alpha. Further analysis revealed that methyl-PGE1 appeared to suppress both the induction and elicitation phases of the cell-mediated response to schistosome eggs. Cyclophosphamide treatment could partially reverse this suppression, but the induction of suppressor cell activity was not solely responsible for this effect. The possible role and mechanism of PGs as modulators of chronic inflammation is discussed.
Animals Antibodies