title: DNFB-DNS hapten-induced colitis in mice should not be considered a model of inflammatory bowel disease.
abstract: BACKGROUND
  The dinitrofluorobenzene/dinitrosulfonic acid (DNFB/DNS) model was originally described as an experimental model of intestinal inflammation resembling human ulcerative colitis (UC). Due to the absence of acceptable UC experimental models for pharmacological preclinical assays, here we examine the immune response induced in this model.
  
  
  METHODS
  Balb/c mice were sensitized by skin application of DNFB on day 1, followed by an intrarectal challenge with DNS on day 5. We further expanded this model by administering a second DNS challenge on day 15. The features of colonic inflammation and immune response were evaluated.
  
  
  RESULTS
  The changes observed in colonic tissue corresponded, in comparison to the trinitrobenzene sulfonic acid (TNBS) colitis model, to a mild mucosal effect in the colon, which spontaneously resolved in less than 5 days. Furthermore, the second hapten challenge did not exacerbate the inflammatory response. In contrast to other studies, we did not observe any clear involvement of tumor necrosis factor alpha (TNF-α) or other Th1 cytokines during the initial inflammatory response; however, we found that a more Th2-humoral response appeared to mediate the first contact with the hapten. An increased humoral response was detected during the second challenge, although an increased Th1/Th17-cytokine expression profile was also simultaneously observed.
  
  
  CONCLUSIONS
  On the basis of these results, although the DNFB/DNS model can display some features found in human UC, it should be considered as a model for the study of the intestinal hypersensitivity seen, for example, during food allergy or irritable bowel syndrome but not intestinal inflammation per se.
authors: Department of Pharmacology, Center for Biomedical Research, University of Granada, Granada, Spain.
authors: Elvira
authors: E
authors: Bailón
authors: Margarita
authors: M
authors: Cueto-Sola
authors: Pilar
authors: P
authors: Utrilla
authors: Ana
authors: A
authors: Nieto
authors: Natividad
authors: N
authors: Garrido-Mesa
authors: Antonio
authors: A
authors: Celada
authors: Antonio
authors: A
authors: Zarzuelo
authors: Jordi
authors: J
authors: Xaus
authors: Julio
authors: J
authors: Gálvez
authors: Mònica
authors: M
authors: Comalada
mesh_terms: D000818:Animals; D001557:Benzenesulfonates / Q000633:toxicity*; D003092:Colitis / Q000139:chemically induced* / Q000276:immunology / Q000473:pathology; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004139:Dinitrofluorobenzene / Q000633:toxicity*; D004195:Disease Models, Animal; D004342:Drug Hypersensitivity; D006241:Haptens / Q000633:toxicity*; D006801:Humans; D007124:Immunoenzyme Techniques; D007249:Inflammation / Q000139:chemically induced* / Q000276:immunology / Q000473:pathology; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D008214:Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008297:Male; D008407:Mast Cells / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C
chemical_list: D001557:Benzenesulfonates; D016207:Cytokines; D006241:Haptens; C007488:dinitrobenzenesulfonic acid; D004139:Dinitrofluorobenzene