title: Microbiota: dual-faceted player in experimental colitis.
abstract: We have recently demonstrated that microbiota stimulation of innate immune pathways is required for T cell spontaneous proliferation and chronic intestinal inflammation. Microbiota promoted spontaneous proliferation of T cells by activating dendritic cells to produce interleukin (IL)-6 via a TLR/Myd88-dependent pathway. Although both CBir1-specific Tcr transgenic (CBir1 Tg) T cells, which are specific for an immunodominant microbiota antigen and OT-II T cells, which are specific for the model antigen ovalbumin, underwent spontaneous proliferation, only CBir1 Tg T cells but not OT-II T cells induced colitis in specific pathogen-free RAG(-/-) mice. Blockade of il-6 or il-6-mediated spontaneous proliferation of CBir1 Tg T cells abrogated colitis induction in this adoptive transfer model. Our data reveal that microbiota serves as a natural adjuvant for T cell spontaneous proliferation and development of chronic intestinal inflammation and that both microbiota stimulation of innate immune cells with subsequent T cell spontaneous proliferation and microbiota antigen activation of antigen-specific Tcr are required for the induction of experimental colitis.
authors.affiliation: Department of Microbiology, University of Texas Medical Branch, Galveston, TX, USA.
authors.forename: Ting
authors.initials: T
authors.lastname: Feng
authors.forename: Charles O
authors.initials: CO
authors.lastname: Elson
authors.forename: Yingzi
authors.initials: Y
authors.lastname: Cong
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D001419:Bacteria / Q000276:immunology* / Q000472:pathogenicity*; D002908:Chronic Disease; D003092:Colitis / Q000382:microbiology* / Q000473:pathology*; D006801:Humans; D015850:Interleukin-6 / Q000276:immunology; D054892:Metagenome / Q000276:immunology*; D051379:Mice; D018345:Mice, Knockout; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D015850:Interleukin-6