Nfib UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Ugt2b5 UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
9030619P08Rik DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Cxcl13 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Analysis of 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '0 day'
Acaa1b UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Ccl20 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Greb1 UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Cldn8 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Colec10 UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Cpn1 UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Prap1 UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
H2-Ob DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Tnni1 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Rgs2 UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Crisp3 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Wdfy1 UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Cd79b DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Car12 UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
(Factor value) GENOTYPE/wild type genotype
Slc37a2 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Clu DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Btla DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Epha7 UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
(Factor value) GENOTYPE/CD4-CRE+ (PPAR g null)
Tsc22d3 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Adra2a UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Ms4a1 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Pcdh17 UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Analysis of 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Pln UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
(Sample) cell type/colonic mucosal CD4+ T cell
Ighm DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Wdfy1 UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '0 day'
Hmgcs2 UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Csta1 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Ces1f UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Capn13 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Ces1g UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Glycam1 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Rps4l DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '0 day'
Ces2a UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
BACKGROUND: Peroxisome proliferator-activated receptor g (PPAR g) is a nuclear receptor whose activation has been shown to modulate macrophage and epithelial cell-mediated inflammation. The objective of this study was to use a systems approach for investigating the mechanism by which the deletion of PPAR g in T cells modulates the severity of dextran-sodium sulfate (DSS)-induced colitis, immune cell distribution and global gene expression. METHODS: Wild-type (WT) or PPAR g flfl; CD4 Cre+ (CD4cre) mice in a C57BL/6 background were challenged with 2.5% DSS in their drinking water for 0, 2, or 7 days. Mice were scored on disease severity both clinically and histopathologically. Flow cytometry was used to assess lymphocyte and macrophage populations in the blood, spleen, and mesenteric lymph nodes (MLN). Global gene expression in colonic mucosa was profiled using Affymetrix microarrays. RESULTS: Both disease severity and inflammation-related body weight loss were accelerated by the deficiency of PPAR g in T cells. Examination of colon histopathology revealed significantly greater epithelial erosion, leukocyte infiltration, and mucosal thickening in the CD4cre mice on day 7. CD4cre mice had more CD8+ T cells than wt mice and fewer CD4+FoxP3+ regulatory T cells (Treg) and IL10+CD4+ T cells in blood and MLN, respectively. Transcriptomic profiling revealed around 3000 genes being transcriptionally altered as a result of DSS challenge in CD4cre mice. These included up-regulated adhesion molecules on day 7 and proinflammatory cytokines interleukin-6 (IL-6) and IL-1b, and suppressor of cytokine signaling 3 (SOCS-3) mRNA expression. CONCLUSIONS: These findings suggest that T cell PPAR g down-regulates inflammation during DSS colitis by inhibiting colonic expression of inflammatory mediators and increasing MLN Treg. Colonic mucosa from wt and CD4cre mice were sampled at 0 (no DSS), 2, and 7 days of DSS-induced experimental colitis
Isx UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Atp12a DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
AI854703 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
(Sample) genotype/CD4-CRE+ (PPAR g null)
Il22ra2 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Etv3 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Slc26a7 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Hkdc1 UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Hoxd13 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Mal UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Mt2 UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Klb DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Prkacb DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Slc35d1 UP in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'
Best2 DOWN in 'CD4-CRE+ (PPAR g null)' vs 'wild type genotype' at '2 day'