Jiangtao Hou1, Xueying Hu2, Bin Chen1, Xu Chen1, Lina Zhao1, Zhuoqun Chen3, Fengbin Liu1, Zhihui Liu4. 1. Department of Gastroenterology, the First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, 510000, China. 2. The First Clinical College, Guangzhou University of Chinese Medicine, Guangzhou, 510000, China. 3. Clinical Skills Center, Guangzhou University of Chinese Medicine, Guangzhou, 510000, China. 4. Department of Laboratory, the First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, 510000, China. Electronic address: 15918884353@139.com.
Abstract
BACKGROUND: Ulcerative 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 RESULTS: Therefore, 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. CONCLUSION: miR-155 seems to target Est-1 and induces UC via the IL-23/17/6-mediated Th17 pathway.
BACKGROUND:Ulcerative 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 RESULTS: Therefore, 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. CONCLUSION:miR-155 seems to target Est-1 and induces UC via the IL-23/17/6-mediated Th17 pathway.