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Am J Physiol Gastrointest Liver Physiol 281: G764-G778, 2001;
0193-1857/01 $5.00
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Vol. 281, Issue 3, G764-G778, September 2001

Helicobacter-induced inflammatory bowel disease in IL-10- and T cell-deficient mice

Andrew Burich1,5, Robert Hershberg3, Kim Waggie4, Weiping Zeng1, Thea Brabb1,2, Gina Westrich5, Joanne L. Viney5, and Lillian Maggio-Price1,5

Departments of 1 Comparative Medicine and 2 Molecular Biotechnology, University of Washington, Seattle 98195; 3 Corixa Corporation, Seattle 98104; 4 Zymogenetics Incorporated, Seattle 98102; and 5 Department of Molecular Immunology, Immunex Corporation, Seattle, Washington 98101

Inflammatory bowel disease (IBD) is thought to result from a dysregulated mucosal immune response to luminal microbial antigens, with T lymphocytes mediating the colonic pathology. Infection with Helicobacter spp has been reported to cause IBD in immunodeficient mice, some of which lack T lymphocytes. To further understand the role of T cells and microbial antigens in triggering IBD, we infected interleukin (IL)-10-/-, recombinase-activating gene (Rag)1-/-, T-cell receptor (TCR)-alpha -/-, TCR-beta -/-, and wild-type mice with Helicobacter hepaticus or Helicobacter bilis and compared the histopathological IBD phenotype. IL-10-/- mice developed severe diffuse IBD with either H. bilis or H. hepaticus, whereas Rag1-/-, TCR-alpha -/-, TCR-beta -/-, and wild-type mice showed different susceptibilities to Helicobacter spp infection. Proinflammatory cytokine mRNA expression was increased in the colons of Helicobacter-infected IL-10-/- and TCR-alpha -/- mice with IBD. These results confirm and extend the role of Helicobacter as a useful tool for investigating microbial-induced IBD and show the importance, but not strict dependence, of T cells in the development of bacterial-induced IBD.

Helicobacter bilis; Helicobacter hepaticus; colitis; proinflammatory cytokines


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