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Home › Dataset Library › Transcription profiling by array of mouse Peroxisome proliferator-activated receptor g (PPARg) null CD4+ T cells after treatment with...

Dataset: Transcription profiling by array of mouse Peroxisome proliferator-activated receptor g (PPARg) null CD4+ T cells after treatment with dextran-sodium sulfate for 2 or 7 days to induce colitis

BACKGROUND: Peroxisome proliferator-activated receptor g (PPAR g) is a nuclear receptor whose activation has been shown to modulate...

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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

Species:
mouse

Samples:
17

Source:
E-GEOD-20523

PubMed:
20537136

Updated:
Dec.12, 2014

Registered:
Nov.11, 2014


Factors: (via ArrayExpress)
Sample genotype time
GSM515496 CD4-CRE+ (PPAR g null) 0
GSM515496 CD4-CRE+ (PPAR g null) 0
GSM515496 CD4-CRE+ (PPAR g null) 0
GSM515499 CD4-CRE+ (PPAR g null) 2
GSM515499 CD4-CRE+ (PPAR g null) 2
GSM515499 CD4-CRE+ (PPAR g null) 2
GSM515502 CD4-CRE+ (PPAR g null) 7
GSM515502 CD4-CRE+ (PPAR g null) 7
GSM515502 CD4-CRE+ (PPAR g null) 7
GSM515505 wild type genotype 0
GSM515505 wild type genotype 0
GSM515505 wild type genotype 0
GSM515508 wild type genotype 2
GSM515508 wild type genotype 2
GSM515508 wild type genotype 2
GSM5155 wild type genotype 7
GSM5155 wild type genotype 7

Tags

  • body
  • cell
  • colitis
  • colon
  • cytokine
  • disease
  • dss
  • epithelial cell
  • interleukin
  • interleukin-6
  • leukocyte
  • lymph
  • lymphocyte
  • macrophage
  • mucosa
  • peroxisome
  • spleen

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