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* Departments of Medicine and Microbiology/Immunology, Dartmouth Medical School, Lebanon, NH 03756;
Department of Parasitology, Institut Pasteur, Paris, France;
Department of Microbiology and Immunology, School of Medicine, Stanford University, Stanford, CA 94305; and
Equipe de Parasitologie Moleculaire, Laboratoire de Glycobiologie Structurale et Fonctionnelle, Centre National de la Recherche Scientifique Unité Mixte de Recherche 8576, Universite des Sciences et Technologies de Lille, Villeneuve d’Ascq, France
The role of specific microbial Ags in the induction of experimental inflammatory bowel disease is poorly understood. Oral infection of susceptible C57BL/6 mice with Toxoplasma gondii results in a lethal ileitis within 7–9 days postinfection. An immunodominant Ag of T. gondii (surface Ag 1 (SAG1)) that induces a robust B and T cell-specific response has been identified and a SAG1-deficient parasite (
sag1) engineered. We investigated the ability of sag1 parasite to induce a lethal intestinal inflammatory response in susceptible mice. C57BL/6 mice orally infected with sag1 parasites failed to develop ileitis. In vitro, the mutant parasites replicate in both enterocytes and dendritic cells. In vivo, infection with the mutant parasites was associated with a decrease in the chemokine and cytokine production within several compartments of the gut-associated cell population. RAG-deficient (RAG1–/–) mice are resistant to the development of the ileitis after T. gondii infection. Adoptive transfer of Ag-specific CD4+ effector T lymphocytes isolated from C57BL/6-infected mice into RAG–/– mice conferred susceptibility to the development of the intestinal disease. In contrast, CD4+ effector T lymphocytes from mice infected with the mutant sag1 strain failed to transfer the pathology. In addition, resistant mice (BALB/c) that fail to develop ileitis following oral infection with T. gondii were rendered susceptible following intranasal presensitization with the SAG1 protein. This process was associated with a shift toward a Th1 response. These findings demonstrate that a single Ag (SAG1) of T. gondii can elicit a lethal inflammatory process in this experimental model of pathogen-driven ileitis.
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