Reconstruction of immune-mediated ion secretion in gut mucosa of the athymic rat.

A defect in an immune-mediated, physiological reaction in the small intestine of congenitally immunosuppressed rats has been identified and corrected by recoupling the immunological trigger in the mucosa with epithelial effector cells. Antigenic challenge of jejunum from euthymic rats sensitized by infection with Trichinella spiralis evoked an anaphylactic response in vitro that was characterized by an elevation in transmural short-circuit current (Isc) and caused by net Cl- secretion. In contrast, jejunum from previously infected athymic counterparts failed to respond electrophysiologically to antigenic stimulation. Passive immunization of athymic rats with anti-Trichinella serum restored jejunal responsiveness to antigen. Jejunal unresponsiveness to antigenic challenge in the athymic rat compared with the euthymic rat was not due to a difference in the duration of exposure to the sensitizing antigens, mast cell numbers, inflammation-related histological changes nor to reduced responsiveness of epithelium to Cl- secretagogues. Because the transduction of the antigenic signal into epithelial ion transport changes in euthymic rats requires IgE, mucosal mast cells, mast cell-derived mediators and enteric nerves, the results support the conclusion that an antibody deficiency is the only functional defect preventing the antigen-induced change in mucosal ion transport in the athymic host.