Modulation of granulomatous inflammation by prostaglandin E. Involvement of mononuclear cells.

The effects of exogenous PGE, administered locally to carrageenan sponge-induced granulomata in rats, have been studied in relation to changes in PGE-like material (PGL) and cell counts in exudates. Levels of PGL achieved a peak within 24h, declining thereafter. Administration of PGE during the acute phase led to irregular slight enhancement of subsequent granuloma formation. In contrast, administration of exogenous PGE to pre-formed granuloma, inhibited its formation. The early administration of PGE1, on day 1, inhibited mononuclear cell counts in 24h exudates. This inhibition was still present in 8 day exudates, together with reduced PGL levels. A significant correlation was also observed between phagocytosing macrophages and PGL levels in 8 day exudates after exogenous PGE1 treatment of pre-formed granuloma, suggesting that the exogenous PGE was inhibiting macrophage function, including PGL production. Further studies are necessary to establish whether the observed pharmacological effects indicate that PGE, released during granulomatous inflammation, modulates the process through actions on infiltrating leucocytes.