Villous atrophy and expulsion of intestinal Trichinella spiralis are mediated by T cells.

The development of villous atrophy and crypt hyperplasia in, and expulsion of nematodes from, the small intestine of the mouse during Trichinella infection is shown to be mediated by T cells. During Trichinella infection, worms initially localise in the anterior half of the small intestine. Their expulsion from here after 6–8 days follows the onset of villous atrophy and crypt hyperplasia in the jejunum and the normal jejunal morphology is restored after complete expulsion of worms from the small intestine at 12–15 days. In thymectomised mice, according to the extent of T-cell depletion, worm localisation is atypical, expulsion is either delayed or absent, and villous atrophy and crypt hyperplasia are either delayed and reduced or absent. The adoptive immunization of infected thymectomised mice with mesenteric lymph node cells (including primed T blasts) from infected donors completely restores the normal host response and enhances the onset of crypt hyperplasia. These findings are discussed in relation to T-cell traffic and delayed-type hypersensitivity in the gut.