Abstract
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.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Colon / metabolism
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Colon / microbiology
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Colon / pathology*
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Cytokines / genetics
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Cytokines / metabolism*
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DNA, Bacterial / analysis
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Feces / chemistry
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Feces / microbiology
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Female
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Genes, RAG-1 / genetics
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Genetic Predisposition to Disease
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Helicobacter / isolation & purification
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Helicobacter / pathogenicity
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Helicobacter Infections / complications*
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Helicobacter Infections / metabolism*
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Helicobacter Infections / pathology
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Histocompatibility Antigens Class II / metabolism
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Inflammatory Bowel Diseases / immunology
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Inflammatory Bowel Diseases / microbiology*
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Inflammatory Bowel Diseases / pathology*
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Interleukin-10 / deficiency
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Interleukin-10 / genetics
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Intestinal Mucosa / metabolism
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Intestinal Mucosa / microbiology
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Intestinal Mucosa / pathology
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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RNA, Messenger / metabolism
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Receptors, Antigen, T-Cell / deficiency
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Receptors, Antigen, T-Cell / genetics
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Species Specificity
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Specific Pathogen-Free Organisms
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T-Lymphocytes / immunology
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T-Lymphocytes / metabolism
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Weight Gain
Substances
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Cytokines
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DNA, Bacterial
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Histocompatibility Antigens Class II
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RNA, Messenger
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Receptors, Antigen, T-Cell
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Interleukin-10