Format

Send to

Choose Destination
Pathol Res Pract. 2017 Oct;213(10):1289-1295. doi: 10.1016/j.prp.2017.08.001. Epub 2017 Aug 25.

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

Author information

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.

KEYWORDS:

Inflammatory bowel disease; Ulcerative colitis; miR-155

PMID:
28888763
DOI:
10.1016/j.prp.2017.08.001
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center