title: Helicobacter-induced inflammatory bowel disease in IL-10- and T cell-deficient mice.
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.
authors.affiliation: Department of Comparative Medicine, University of Washington, Seattle 98195, USA.
authors.forename: A
authors.initials: A
authors.lastname: Burich
authors.forename: R
authors.initials: R
authors.lastname: Hershberg
authors.forename: K
authors.initials: K
authors.lastname: Waggie
authors.forename: W
authors.initials: W
authors.lastname: Zeng
authors.forename: T
authors.initials: T
authors.lastname: Brabb
authors.forename: G
authors.initials: G
authors.lastname: Westrich
authors.forename: J L
authors.initials: JL
authors.lastname: Viney
authors.forename: L
authors.initials: L
authors.lastname: Maggio-Price
mesh_terms: D000818:Animals; D003106:Colon / Q000378:metabolism / Q000382:microbiology / Q000473:pathology*; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D004269:DNA, Bacterial / Q000032:analysis; D005243:Feces / Q000737:chemistry / Q000382:microbiology; D005260:Female; D016654:Genes, RAG-1 / Q000235:genetics; D020022:Genetic Predisposition to Disease; D016998:Helicobacter / Q000302:isolation & purification / Q000472:pathogenicity; D016481:Helicobacter Infections / Q000150:complications* / Q000378:metabolism* / Q000473:pathology; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D015212:Inflammatory Bowel Diseases / Q000276:immunology / Q000382:microbiology* / Q000473:pathology*; D016753:Interleukin-10 / Q000172:deficiency / Q000235:genetics; D007413:Intestinal Mucosa / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D012333:RNA, Messenger / Q000378:metabolism; D011948:Receptors, Antigen, T-Cell / Q000172:deficiency / Q000235:genetics; D013045:Species Specificity; D013047:Specific Pathogen-Free Organisms; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D015430:Weight Gain
chemical_list: D016207:Cytokines; D004269:DNA, Bacterial; D000949:Histocompatibility Antigens Class II; D012333:RNA, Messenger; D011948:Receptors, Antigen, T-Cell; D016753:Interleukin-10