Cytokine expression and the role of Thl7 cells in mice colitis

Hepatogastroenterology. 2012 Sep;59(118):1809-13.

Abstract

Background/aims: To explore the expression and mechanism of Thl7 cells and cytokines in mice model with 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced inflammatory bowel disease (IBD).

Methodology: ELISA assay was used to detect the expression of Th17 cytokine IL-17 and Thl cytokines IFN-y in colon tissues. Western blot assay was applied to detect IL-17 expression in peripheral blood mononuclear cells (PBMC), spleen mononuclear cells (SMC), mesenteric lymph node cells and colon tissue of colitic mice. RT-PCR assay was used to detect the effect of anti-IL-17 antibody application on TNF-a, IFN-y and IL-6 mRNA levels in SMCs from colitic mice.

Results: Th17 cytokine IL-17 and Thl cytokines IFN-y were both expressed at high level in TNBS-induced colitic mice. In addition, the expression of Thl7 cytokine appeared earlier than the Thl cytokine. IL-17 levels in SMCs, mesenteric lymph node cells and colon tissue of the disease model group had significant differences compared with normal control group (p<0.01), while the IL-17 level in PBMCs of the disease model group had no significant difference (p>0.05) to control group. After application of 10 ug/mL anti-IL-7 antibody, the TNF-ct, IL-6 and IFN-y mRNA levels in SMCs of the model group showed no significant difference from that of no antibody group (p>0.05).

Conclusions: Both Th17 cells and Thl cells involved in TNBS-induced IBD and the role of Thl17 cells may be through inducing the secretion of pro-inflammatory cytokines.

MeSH terms

  • Animals
  • Antibodies / pharmacology
  • Blotting, Western
  • Cells, Cultured
  • Colitis / blood
  • Colitis / chemically induced
  • Colitis / genetics
  • Colitis / immunology*
  • Colon / drug effects
  • Colon / immunology*
  • Cytokines / blood
  • Cytokines / genetics
  • Cytokines / metabolism*
  • Disease Models, Animal
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Gene Expression Regulation
  • Inflammation Mediators / blood
  • Inflammation Mediators / metabolism*
  • Leukocytes, Mononuclear / immunology
  • Mice
  • Mice, Inbred BALB C
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction
  • Spleen / immunology
  • Th1 Cells / immunology
  • Th17 Cells / drug effects
  • Th17 Cells / immunology*
  • Time Factors
  • Trinitrobenzenesulfonic Acid

Substances

  • Antibodies
  • Cytokines
  • Inflammation Mediators
  • RNA, Messenger
  • Trinitrobenzenesulfonic Acid