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

• Published in: American journal of physiology: Gastrointestinal and liver physiology 2001-09, Vol.281 (3), p.G764-G778
• Main Authors: Burich, A, Hershberg, R, Waggie, K, Zeng, W, Brabb, T, Westrich, G, Viney, J L, Maggio-Price, L
• Format: Article
• Language: English
• Subjects: Animals; Colon - metabolism; Colon - microbiology; Colon - pathology; Cytokines - genetics; Cytokines - metabolism; DNA, Bacterial - analysis; Feces - chemistry; Feces - microbiology; Female; Genes, RAG-1 - genetics; Genetic Predisposition to Disease; Helicobacter - isolation & purification; Helicobacter - pathogenicity; Helicobacter Infections - complications; Helicobacter Infections - metabolism; Helicobacter Infections - pathology; Histocompatibility Antigens Class II - metabolism; Inflammatory Bowel Diseases - immunology; Inflammatory Bowel Diseases - microbiology; Inflammatory Bowel Diseases - pathology; Interleukin-10 - deficiency; Interleukin-10 - genetics; Intestinal Mucosa - metabolism; Intestinal Mucosa - microbiology; Intestinal Mucosa - pathology; Mice; Mice, Inbred C57BL; Mice, Knockout; Receptors, Antigen, T-Cell - deficiency; Receptors, Antigen, T-Cell - genetics; RNA, Messenger - metabolism; Species Specificity; Specific Pathogen-Free Organisms; T-Lymphocytes - immunology; T-Lymphocytes - metabolism; Weight Gain
• ISSN: 0193-1857; 1522-1547
• DOI: 10.1152/ajpgi.2001.281.3.g764

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.