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Blockade of IL-6 signal exacerbates acute inflammatory bowel disease via inhibiting IL-17 producing in activated CD4+ Th17 population.
Blockade of IL-6 signal exacerbates acute inflammatory bowel disease via inhibiting IL-17 producing in activated CD4+ Th17 population.
- Source :
- European Review for Medical & Pharmacological Sciences; Dec2013, Vol. 17 Issue 24, p3291-3295, 5p
- Publication Year :
- 2013
-
Abstract
- BACKGROUND: Inflammatory bowel disease (IBD) is a common disease in human resulted from a various of factors including genetic background, immune system and environment factors. OBJECTIVES: Recent studies suggest pro-inflammatory cytokine IL-17 producing cell subset was involved in the disease development and the maintenance of IBD. And the differentiated and activation of IL-17 producing cells were mostly dependent on the cytokines profile secreted by innate cells in intestinal tissues. In this study, we examined the functions of IL-6 signal in regulatory of IL-17 production in acute IBD model. MATERIALS AND METHODS: Wildtype mice were treated with anti-IL-6 neutralizing antibodies to block IL-6 signal And then treated with DSS to induce acute IBD. RESULTS: Mice treated with anti-IL-6 neutralizing antibodies show severe colitis and high level of pro-inflammatory cytokine IL-17 production in DSS-induced acute IBD model when compared with control group. Our research suggested blockade of IL-6 signal pathways in acute colitus model resulted in specifical activation of IL-17 producing cell population. Furthermore, CD44+ activated Th17 cell population and CD44- IL-17 producing T cells exhibited different susceptibility to IL-6 signal in our model. CONCLUSIONS: Blockade of IL-6 signal in DSS-induced acuted IBD model increased IL-17 production level specifically in CD44- T cells and reduced CD44+ Th17 cell population. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 11283602
- Volume :
- 17
- Issue :
- 24
- Database :
- Supplemental Index
- Journal :
- European Review for Medical & Pharmacological Sciences
- Publication Type :
- Academic Journal
- Accession number :
- 93387426