title: Comparative analysis of colonic gene expression of three experimental colitis models mimicking inflammatory bowel disease.
abstract: BACKGROUND
  Mouse models of inflammatory bowel diseases (IBD) are used to unravel the pathophysiology of IBD and to study new treatment modalities, but their relationship to Crohn's disease (CD) or ulcerative colitis (UC) is speculative.
  
  
  METHODS
  Using Agilent mouse TOX oligonucleotide microarrays, we analyzed colonic gene expression profiles in three widely used models of experimental colitis. In 2 of the models (TNBS and DSS-induced colitis), exogenous agents induce the colitis. In the third model the colitis is induced after transfer of a T-cell population (CD4(+)CD45RB(high) T cells) that lacks regulatory cells into an immunodeficient host.
  
  
  RESULTS
  Compared with control mice, in DSS, TNBS, and the CD45RB transfer colitis mice, 387, 21, and 582 genes were more than 2-fold upregulated in the intestinal mucosa. Analyses of exclusively shared gene expression profiles between the different models revealed that DSS/transfer colitis share 69 concordantly upregulated genes, DSS/TNBS 6, and TNBS/transfer colitis 1. Seven genes were upregulated in all three models. The CD45RB transfer model expression profile included the most genes that are known to be upregulated in IBD. Of 32 genes that are known to change transcriptional activity in IBD (TNF, IFN-gamma, Ltbeta, IL-6, IL-16, IL-18R1, IL-22, CCR2, 7, CCL2, 3, 4, 5, 7, 11, 17, 20, CXCR3, CXCL1, 5, 10, Mmp3, 7,9, 14, Timp1, Reg3gamma, and Pap, S-100a8, S-100a9, Abcb1, and Ptgs2), 2/32 are upregulated in TNBS, 15/32 are upregulated or downregulated in DSS and 30/32 are upregulated or downregulated in the CD45RB transfer colitis.
  
  
  CONCLUSIONS
  The pattern of gene expression in the CD45RB transfer model most closely reflects altered gene expression in IBD.
authors.affiliation: Center of Experimental and Molecular Medicine, AMC, Amsterdam, The Netherlands. a.a.tevelde@amc.uva.nl
authors.forename: Anje A
authors.initials: AA
authors.lastname: te Velde
authors.forename: Floor
authors.initials: F
authors.lastname: de Kort
authors.forename: Ellen
authors.initials: E
authors.lastname: Sterrenburg
authors.forename: Inge
authors.initials: I
authors.lastname: Pronk
authors.forename: Fiebo J W
authors.initials: FJ
authors.lastname: ten Kate
authors.forename: Daniel W
authors.initials: DW
authors.lastname: Hommes
authors.forename: Sander J H
authors.initials: SJ
authors.lastname: van Deventer
mesh_terms: D000818:Animals; D003092:Colitis / Q000139:chemically induced; D016264:Dextran Sulfate; D004195:Disease Models, Animal; D005260:Female; D015870:Gene Expression; D015212:Inflammatory Bowel Diseases / Q000235:genetics*; D017493:Leukocyte Common Antigens / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D016513:Mice, SCID; D020411:Oligonucleotide Array Sequence Analysis; D013601:T-Lymphocytes / Q000276:immunology / Q000637:transplantation; D014302:Trinitrobenzenesulfonic Acid
chemical_list: D014302:Trinitrobenzenesulfonic Acid; D016264:Dextran Sulfate; D017493:Leukocyte Common Antigens