SUPPRESSION BY TRYPANOSOMA-BRUCEI OF ANAPHYLAXIS-MEDIATED ION-TRANSPORT IN THE SMALL-INTESTINE OF RATS

The hypothesis that failure of hosts infected with Trypanosoma brucei to express type 1 hypersensitivity is related to this parasite's abili ty to down-regulate IgE production, and not to an innate lack of aller genicity of T brucei antigens, was tested by studying anaphylaxis-indu ced changes in net epithelial ion transport in rats. Transport changes were quantified electrophysiologically in vitro, as a change in trans mural short-circuit current when sensitized intestine was challenged w ith homologous antigen. Rats injected parenterally with trypanosome an tigen elicited intestinal anaphylaxis in response to antigenic challen ge, whereas the intestine of rats infected with T. brucei failed to re spond. Infection with T. brucei also suppressed the anaphylactic respo nse in rats sensitized to and challenged with ovalbumin and T.spiralis -derived antigens. In these cases suppression was related to the abili ty of T. brucei to block production of IgE, and not to the physiologic al failure of the epithelial response. However, in rats sensitized by infection with T, spiralis, neither the anaphylactic response nor IgE production were inhibited by T. brucei. Furthermore, intestinal mastoc ytosis normally associated with trichinosis was unaffected by the tryp anosome infection. Results support the conclusion that the failure to express anaphylaxis in T. brucei-infected rats is due to the inhibitio n of IgE production and not to the lack of allergenicity of trypanosom e antigens.