In vitro and in vivo Inhibition of Mast Cell Degranulation by a Factor from Schistosoma mansoni

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Abstract
Schistosome incubation product (SIP) obtained from Schistosoma mansoni was tested on mast cell degranulation in vitro or in vivo elicited by chemical compounds or anaphylactic reactions. Normal mast cells from Wistar rats were labeled with 3H-serotonin and incubated with the SIP. Serotonin release normally induced by the chemical compounds 48/80, polymyxin B or an anaphylactic system (ovalbumin-antiovalbumin) was inhibited when mast cells were preincubated with the SIP. Cutaneous reactions elicited by the compound 48/80 or polymyxin B and passive or active cutaneous anaphylactic reactions, were inhibited by the intradermal injection of the SIP before the challenge. The anaphylactic shock by ovalbumin was also inhibited in guinea pigs by a previous intraperitoneal injection of the SIP. This inhibitor appeared dialysable, heat resistant and soluble in trichloroacetic acid (TCA). The inhibitory activity was found in the fraction eluted from an antischistosome immunosorbent. However, no inhibition of cutaneous reactions was observed with the circulating (TCA-soluble, thermostable) M antigen previously described and purified from schistosomes. No effect of the SIP was observed on the growth of HeLa cells or the J 111 human monocytic cell line. The increase of intracellular cAMP levels in mast cells incubated with the SIP suggests that modulation of cAMP is involved in the mechanism of inhibition. The SIP inhibited also the mast cell-dependent eosinophil cytotoxicity for schistosomula sensitized with IgG2a antibody. The SIP appeared to act selectively on mast cell degranulation without effect on eosinophils or the mast cell mediators. This inhibitor, denominated schistosome-derived inhibitory factor, released by the parasite, which acts on mast cells could partly explain the low incidence of clinical allergic manifestations observed in parasitic diseases and might represent an escape mechanism of the parasite to the antibody-dependent eosinophil cytotoxicity mechanism.