miR-155 targets Est-1 and induces ulcerative colitis via the IL-23/17/6-mediated Th17 pathway

Publication date: Available online 25 August 2017
Source:Pathology - Research and Practice
Author(s): Jiangtao Hou, Bin Chen, Xueying Hu, Xu Chen, Lina Zhao, Zhuoqun Chen, Fengbin Liu, Zhihui Liu
BackgroundUlcerative colitis (UC) is a type of inflammatory bowel disease (IBD) affecting millions of people worldwide. miR-155 has been reported to be upregulated in various inflammatory diseases and is a positive regulator of the T-cell response. IL-17 secreting helper T (Th17) cells have been heavily implicated in tissue-specific immune pathology, including UC.Methods and resultsTherefore, we targeted miR-155 and investigated its expression levels in a DSS-induced UC mouse model, revealing increased expression. Est-1 expression was found to have decreased, but the levels of IL-23/17/6 were raised significantly and Th17 had experienced an obvious increase. We overexpressed miR-155 using a lentiviral treatment. Increased miR-155 expression induced a more severe damage to colon tissues. In this case, the level of Est-1 decreased even further, thereby enhancing IL-23/17/6-mediated Th17 differentiation.ConclusionmiR-155 seems to target Est-1 and induces UC via the IL-23/17/6-mediated Th17 pathway.



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