Elimination of a primary schistosome infection from rats coincides with elevated IgE titres and mast cell degranulation

Abstract

Schistosomes are eliminated from laboratory rats around 28 days post-infection, whilst they are still resident within the hepatic portal distributaries of the liver. We have previously shown that their presence in this location is accompanied by an intense mastocytosis. We have investigated the potential relationships between IgE responses, the allergenicity of schistosome antigens, mast cell responsiveness, and worm elimination. Total and specific IgE were measured using an ELISA and a functional assay based on 3H serotonin release from activated rat basophilic leukemia cells (RBL-SRA), respectively. Both assays revealed that infected rats produced elevated IgE titres relative to naive animals. At days 28 and 35, mixed-sex infections stimulated a higher total IgE than male-only infections. IgE was affinity purified from rat infection serum and used to probe a fractionated soluble worm antigen preparation (SWAP) by Western blotting. Two allergenic products were detected of M(r) 67 and 36-38 kDa, the former having the same molecular weight as a previously identified secretory protein. IgE from mixed-sex schistosome infections bound strongly to the 36-38 kDa molecule, compared to the relatively weak binding exhibited by IgE from male-only infection serum. Since eggs were not recovered from the infected rats, this reactivity was attributed to the greater release of allergens from female worms. Results from the RBL-SRA showed that female SWAP was a more effective trigger of mast cell degranulation in vitro, for equal amounts of protein. This enhanced allergenicity was ascribed to the relative abundance of carbohydrate moieties. Our results support a role for IgE, and mast cell degranulation in the elimination of a primary schistosome burden from rats.

Manson's schistosomiasis in the undernourished mouse: some recent findings

“…Nevertheless, there is considerable controversy concerning the role of IgE in the host-parasite relationship based on the work in humans and other experimental models (Hagan 1993, Capron & Capron 1994, Cutts & Wilson 1997, Webster et al 1997. Controversial findings have also been published concerning the biological role of IgE within the experimental model of the primary murine S. mansoni infection (Amiri et al 1994).…”

Production of interferon‐γ by natural killer cells and aging in chronic human schistosomiasis

“…It is possible that other Th1 cytokines, such as tumor necrosis factor-a (TNF-a), or humoral immune responses, such as specific IgE production, also act as important players in the acquired immunity to S. mansoni in young and middle-aged negative individuals. Some authors have already suggested a protective role for specific IgE in experimental models of infection with S. mansoni 32,33 and in human schistosomiasis. 34 Others have found no correlation between specific IgE and resistance to infection.…”

An overview of animal models in experimental schistosomiasis and refinements in the use of non-human primates

“…T his schistosome attri tion is im mune-mediated and the antibody dependent cell-mediated cytotoxicity mechanism plays a major role (Capron & Capron 1994 ). Parasite elimination in the rat coincides with eosinophilia, elevated IgE in circulation and mast cell degranulati on (Cutts & Wilson 1997 ). Furtherm ore, passive transfer experiments using monoclonal IgE antibody have con®rmed in vivo the ef®cacy of IgE in this protection (Verwaerde e t a l. 1987 ).…”