Th17 Responses Are not Induced in Dextran Sodium Sulfate Model of Acute Colitis
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Dextran sodium sulfate (DSS) is a widely used chemical model for inflammatory bowel disease (IBD). It is thought that imbalances in the T helper (Th) cell subsets contribute to IBD. Recent studies suggest that the acute DSS-colitis model is polarized toward a Th1/Th17 profile based on RT-PCR analysis of colonic tissues. In the current study we determined whether colonic Th cells from DSS-colitis mice were skewed toward the Th17 profile. Mice were treated with 5% DSS for 7 days and colonic T cells isolated and examined for production of IFN-γ (Th1 cell), IL-4 (Th2 cell) and IL-17 (Th17 cell) by intracellular flow cytometry. We found that the percentage of colonic Th17 cells were similar to non-treated controls but the percentage of Th1 cells were elevated in DSS-colitis mice. These results suggest that in the acute DSS-colitis model the colonic Th cells exhibit a Th1profile and not a Th17 profile.
Abstract
Dextran sodium sulfate (DSS) is a widely used chemical model for inflammatory bowel disease (IBD). It is thought that imbalances in the T helper (Th) cell subsets contribute to IBD. Recent studies suggest that the acute DSS-colitis model is polarized toward a Th1/Th17 profile based on RT-PCR analysis of colonic tissues. In the current study we determined whether colonic Th cells from DSS-colitis mice were skewed toward the Th17 profile. Mice were treated with 5% DSS for 7 days and colonic T cells isolated and examined for production of IFN-γ (Th1 cell), IL-4 (Th2 cell) and IL-17 (Th17 cell) by intracellular flow cytometry. We found that the percentage of colonic Th17 cells were similar to non-treated controls but the percentage of Th1 cells were elevated in DSS-colitis mice. These results suggest that in the acute DSS-colitis model the colonic Th cells exhibit a Th1profile and not a Th17 profile.
참고문헌 (19)
- Xavier RJ, "Unravelling the pathogenesis of inflammatory bowel disease", Nature, 448, pp.427~434 (2007)
- Strober W, "The fundamental basis of inflammatory bowel disease", J Clin Invest, 117, pp.514~521 (2007)
- Strober W, "Why study animal models of IBD", Inflamm Bowel Dis, 14(2), pp.S129~S131 (2008)
- Okayasu I, "A novel method in the induction of reliable experimental acute and chronic ulcerative colitis in mice", Gastroenterology, 98, pp.694~702 (1990)
- Pizarro TT, "Cytokine therapy for Crohn's disease: advances in translational research", Annu Rev Med, 58, pp.433~444 (2007)
- Fuss IJ, "Both IL-12p70 and IL-23 are synthesized during active Crohn's disease and are down-regulated by treatment with anti-IL-12 p40 monoclonal antibody", Inflamm Bowel Dis, 12, pp.9~15 (2006)
- Alex P, "Distinct cytokine patterns identified from multiplex profiles of murine DSS and TNBS-induced colitis", Inflamm Bowel Dis, 15, pp.341~352 (2009)
- 이기종, "A human colonic commensal promotes colon tumorigenesis via activation of T helper type 17 T cell responses", Nature Medicine, 15(9), pp.1016~1022
- Brown JB, "P-selectin glycoprotein ligand-1 is needed for sequential recruitment of T-helper 1 (Th1) and local generation of Th17 T cells in dextran sodium sulfate (DSS) colitis", Inflamm Bowel Dis (2011)
- Sanada Y, "Therapeutic effects of novel sphingosine-1-phosphate receptor agonist W-061 in murine DSS colitis", PLoS One, 6, pp.e23933~ (2011)
- Nuñez-Andrade N, "P-selectin glycoprotein ligand-1 modulates immune inflammatory responses in the enteric lamina propria", J Pathol, 224, pp.212~221 (2011)
- Ito R, "Involvement of IL-17A in the pathogenesis of DSS-induced colitis in mice", Biochem Biophys Res Commun, 377, pp.12~16 (2008)
- Egger B, "Characterisation of acute murine dextran sodium sulphate colitis: cytokine profile and dose dependency", Digestion, 62, pp.240~248 (2000)
- Nam JS, "Transforming growth factor beta subverts the immune system into directly promoting tumor growth through interleukin-17", CANCER RESEARCH, 68(10), pp.3915~3923 (2008), AMER ASSOC CANCER RESEARCH
- Pichavant M, "Ozone exposure in a mouse model induces airway hyperreactivity that requires the presence of natural killer T cells and IL-17", J Exp Med, 205, pp.385~393 (2008)
- Rachitskaya AV, "Cutting edge: NKT cells constitutively express IL-23 receptor and RORgammat and rapidly produce IL-17 upon receptor ligation in an IL-6-independent fashion", J Immunol, 180, pp.5167~5171 (2008)
- Ferretti S, "IL-17, produced by lymphocytes and neutrophils, is necessary for lipopolysaccharide-induced airway neutrophilia: IL-15 as a possible trigger", J Immunol, 170, pp.2106~2112 (2003)
- Takahashi N, "IL-17 produced by Paneth cells drives TNF-induced shock", J Exp Med, 205, pp.1755~1761 (2008)
- Duan J, "Microbial colonization drives expansion of IL-1 receptor 1-expressing and IL-17-producing gamma", delta T cells, 2010, pp.7, 140~150