title: Murine Trinitrobenzoic Acid-Induced Colitis as a Model of Crohn's Disease.
abstract: Inflammatory Bowel Diseases, Crohn's disease and ulcerative colitis, result from the uncontrolled inflammation that occurs in genetically susceptible individuals and the dysregulation of the innate and adaptive immune systems. The response of these immune systems to luminal gut microbiota and their products results in altered intestinal permeability, loss of barrier function, and mucosal inflammation and ulceration. Animal models of experiment intestinal inflammation have been developed that leverage the development of spontaneous inflammation in certain mouse strains, e.g. Samp1/Yit mice, or induction of inflammation using gene-targeting e.g. IL-10 null mice, administration of exogenous agents e.g. DSS, or adoptive transfer of T-cells into immunodeficient mice, e.g. CD4(+) CD45Rb(Hi) T-cell transfer. Colitis induced by rectal instillation of the haptenizing agent, 2,4,6 trinitrobenzene sulfonic acid, is one of the most commonly used and well-characterized models of Crohn's disease in humans.
authors.affiliation: Division of Gastroenterology, Hepatology and Nutrition, Medical College of Virginia Campus, Virginia Commonwealth University, Molecular Medicine Research Building 5-031, P.O. Box 980341, Richmond, VA, 23298-0341, USA. john.kuemmerle@vcuhealth.org.
authors.forename: John F
authors.initials: JF
authors.lastname: Kuemmerle
mesh_terms: D056704:Adaptive Immunity; D000818:Animals; D003092:Colitis / Q000139:chemically induced* / Q000276:immunology; D003424:Crohn Disease / Q000139:chemically induced* / Q000276:immunology; D004195:Disease Models, Animal; D000069196:Gastrointestinal Microbiome; D006801:Humans; D007113:Immunity, Innate; D051379:Mice; D018345:Mice, Knockout; D014302:Trinitrobenzenesulfonic Acid / Q000009:adverse effects*
chemical_list: D014302:Trinitrobenzenesulfonic Acid
keywords: Inflammatory bowel disease; T Cell-mediated colitis