Macrophages as targets of inhibitory effects of E-type prostaglandins in immune-related inflammation.
The anti-inflammatory effects of E-prostaglandins (PGE) are attracting interest because they are mediated through actions on cells which are also targets for the putative immunomodulator functions of PGE. In the majority of experimental inflammatory conditions, in which inhibitory effects of PGE have been demonstrated, a variety of immunocytes are implicated, including diverse lymphocyte populations. The inhibitory effects of PGE, however, are also readily observable on the tissue component of the carrageenin-induced granuloma (an immune-related inflammatory model) in which activated macrophages, but not lymphocytes participate. Granuloma-derived macrophages are particularly interesting cells for the study of responsiveness to PGE, because the results obtained on such cells in vitro are directly related to the anti-inflammatory effects of PGE on the macrophage phase of the granuloma in vivo. Such combined studies have revealed differences between the responsiveness of granuloma macrophages to PGE2 and prostacyclin, while with elicited peritoneal macrophages such a difference could not be observed. The adenylate cyclase in granuloma macrophages appears to be unusually sensitive to activation by PGE2, but insensitive to prostacyclin.
D000818:Animals; D000242:Cyclic AMP / Q000502:physiology; D006099:Granuloma / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D008214:Lymphocytes / Q000503:physiopathology; D008264:Macrophages / Q000276:immunology*; D011458:Prostaglandins E / Q000502:physiology*
D011458:Prostaglandins E; D000242:Cyclic AMP