Abstract

Immunologically mediated expulsion of Trichinella spiralis infective larvae in the rat was used as a model to test the hypothesis that intestinal anaphylaxis induced by parasite antigen causes ion transport alterations in small intestinal epithelium, and that the small intestinal epithelium, by altering its physiologic state in response to mast cell-derived mediators, functions as an effector tissue in the expulsion process. Experimental results demonstrated that the rapid rejection response and antigen-inducible changes in net intestinal ion transport acquired through active immunization were transferable with serum containing a high titer of anti-trichinella homocytotropic antibody, as measured by the PCA test. Neither response was expressed in nonimmune hosts nor in recipients of serum in which the PCA-detectable antibody was reduced by heat treatment. Net ion transport by jejunal epithelium of both actively and passively immunized rats was measured in Ussing chambers by using the electrical correlate, short circuit current (Isc). Involvement of chloride secretion in antigen-induced alterations in Isc was deduced from the use of chemical agents that effectively and specifically blocked the antigen-induced Cl- secretory response. The results implicate anaphylaxis in both rapid worm rejection and altered epithelial ion transport.

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