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Granulomatous hypersensitivity to Schistosoma mansoni EGG antigens in human schistosomiasis. IV. A role for prostaglandin‐induced inhibition of in vitro granuloma formation
Author(s) -
GOES ALFREDO M.,
REZENDE SIMONE A.,
GAZZINELLI GIOVANNI,
DOUGHTY BARBARA L.
Publication year - 1994
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.1994.tb00299.x
Subject(s) - schistosoma mansoni , granuloma , immune system , biology , immunology , antigen , schistosomiasis , macrophage , in vitro , delayed hypersensitivity , macrophage migration inhibitory factor , cytokine , helminths , biochemistry
SUMMARY The prostaglandins (PG) are known to regulate immune cell function(s) and participate in the progression of both acute and chronic inflammatory reactions. Using an in vitro model of Schistosoma mansoni egg‐induced hypersensitivity granulomas, we have delineated the role of immune complexes (IC) in the induction and release of PG and their inhibitory effects on granuloma development. The hypersensitivity‐type granuloma reaction to soluble egg antigen (SEA) was examined using a model of in vitro granuloma formation. Our results show that granuloma formation was dramatically suppressed by the addition to the granuloma cultures of IC, PGE 1 , PGE 2 , while PGF 2 alpha had no significant effect. The inhibition of the PG function was achieved by the introduction of anti‐PG antibodies that blocked suppression of granuloma formation. It appears in this model system that IC may inhibit the activity of granuloma formation by stimulating the monocyte‐macrophage lineage to release inhibitory mediators. Our results suggest that the prostaglandins E series may be important in the generation and maintenance of suppression of the granulomatous inflammatory response to S. mansoni egg antigens.