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

Inflammatory bowel disease (IBD) is thought to result from a dysregulated m ucosal immune response to luminal microbial antigens, with T lymphocytes me diating the colonic pathology. Infection with Helicobacter spp has been rep orted to cause IBD in immunodeficient mice, some of which lack T lymphocyte s. To further understand the role of T cells and microbial antigens in trig gering IBD, we infected interleukin (IL)-10(-/-), recombinase-activating ge ne (Rag)1(-/-), T-cell receptor (TCR)-alpha (-/-), TCR-beta (-/-), and wild type mice with Helicobacter hepaticus or Helicobacter bilis and compared th e histopathological IBD phenotype. IL-10(-/-) mice developed severe diffuse IBD with either H. bilis or H. hepaticus, whereas Rag1(-/-), TCR-alpha (-/ -), TCR-beta-/-, and wildtype mice showed different susceptibilities to Hel icobacter spp infection. Proinflammatory cytokine mRNA expression was incre ased 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 importa nce, but not strict dependence, of T cells in the development of bacterial- induced IBD.