title: The potential protective role of caveolin-1 in intestinal inflammation in TNBS-induced murine colitis.
abstract: BACKGROUND
  Caveolin-1 (Cav-1) is a multifunctional scaffolding protein serving as a platform for the cell's signal-transduction and playing an important role in inflammation. However, its role in inflammatory bowel disease is not clear. A recent study showed that Cav-1 is increased and mediates angiogenesis in dextran sodium sulphate-induced colitis, which are contradictory to our pilot findings in 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis. In the present study, we further clarified the role of Cav-1 in TNBS-induced colitis.
  
  
  METHODS
  In BALB/c mice, acute colitis was induced by intra-rectal administration of one dose TNBS, while chronic colitis was induced by administration of TNBS once a week for 7 weeks. To assess the effects of complete loss of Cav-1, Cav-1 knockout (Cav-1-/-) and control wild-type C57 mice received one TNBS administration. Body weight and clinical scores were monitored. Colon Cav-1 and pro-inflammatory cytokine levels were quantified through ELISAs. Inflammation was evaluated through histological analysis.
  
  
  RESULTS
  Colon Cav-1 levels were significantly decreased in TNBS-induced colitis mice when compared to normal mice and also inversely correlated with colon inflammation scores and proinflammatory cytokine levels (IL-17, IFN-γ and TNF) significantly. Furthermore, after administration of TNBS, Cav-1-/- mice showed significantly increased clinical and colon inflammatory scores and body weight loss when compared with control mice.
  
  
  CONCLUSIONS
  Cav-1 may play a protective role in the development of TNBS-induced colitis. Our findings raise an important issue in the evaluation of specific molecules in animal models that different models may exhibit opposite results because of the different mechanisms involved.
authors.affiliation: Department of Immunology, University of Manitoba, Winnipeg, Manitoba, Canada; Department of Pediatrics and Child Health, University of Manitoba, Winnipeg, Manitoba, Canada.
authors.forename: Carolyn R
authors.initials: CR
authors.lastname: Weiss
authors.affiliation: Department of Immunology, University of Manitoba, Winnipeg, Manitoba, Canada; Department of Pediatrics and Child Health, University of Manitoba, Winnipeg, Manitoba, Canada.
authors.forename: Qingdong
authors.initials: Q
authors.lastname: Guan
authors.affiliation: Department of Pediatrics and Child Health, University of Manitoba, Winnipeg, Manitoba, Canada.
authors.forename: Yanbing
authors.initials: Y
authors.lastname: Ma
authors.affiliation: Department of Pathology, University of Manitoba, Winnipeg, Manitoba, Canada.
authors.forename: Gefei
authors.initials: G
authors.lastname: Qing
authors.affiliation: Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada; IBD Clinical and Research Centre, University of Manitoba, Winnipeg, Manitoba, Canada.
authors.forename: Charles N
authors.initials: CN
authors.lastname: Bernstein
authors.affiliation: Department of Immunology, University of Manitoba, Winnipeg, Manitoba, Canada; Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Warrington
authors.affiliation: Department of Immunology, University of Manitoba, Winnipeg, Manitoba, Canada; Department of Pediatrics and Child Health, University of Manitoba, Winnipeg, Manitoba, Canada.
authors.forename: Zhikang
authors.initials: Z
authors.lastname: Peng
mesh_terms: D000818:Animals; D051242:Caveolin 1 / Q000502:physiology*; D003092:Colitis / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism*; D003094:Collagen / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D005260:Female; D008297:Male; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D014302:Trinitrobenzenesulfonic Acid
chemical_list: D051242:Caveolin 1; D016207:Cytokines; D014302:Trinitrobenzenesulfonic Acid; D003094:Collagen