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KT2 alleviates ulcerative colitis by reducing Th17 cell differentiation through the miR-302c-5p/STAT3 axis
Dandan Gu1, Qiong Nan1, Yinglei Miao1
1Department of Gastroenterology, The First Affiliated Hospital of Kunming Medical University, Yunnan Province Clinical Research Center for Digestive Diseases, Kunming, Yunnan 650032, China.
European Journal of Cell Biology
|April 11, 2022
Summary
KT2, an antimicrobial peptide, alleviates ulcerative colitis (UC) by inhibiting Th17 cell differentiation. This occurs via the miR-302c-5p/STAT3 pathway, offering a potential therapeutic strategy for UC.
Area of Science:
- Immunology
- Gastroenterology
- Molecular Biology
Background:
- Abnormal T helper 17 (Th17) cell differentiation exacerbates ulcerative colitis (UC).
- Antimicrobial peptides (AMPs) offer protection against UC.
- The role of cationic AMP KT2 in UC was previously unknown.
Purpose of the Study:
- To investigate the function and mechanism of KT2 in ulcerative colitis.
- To determine KT2's effect on Th17 cell differentiation in UC models.
Main Methods:
- Established a UC mouse model using dextran sulfate sodium and administered KT2.
- Assessed KT2's impact on Th17 cell differentiation in vivo and in vitro.
- Utilized molecular techniques including qPCR, loss-of-function assays, and dual-luciferase reporter assays to elucidate the mechanism.
Main Results:
- KT2 significantly restrained Th17 cell differentiation and slowed UC progression in both models.
- KT2 elevated miR-302c-5p expression, which inhibited Th17 cell differentiation.
- KT2 suppressed STAT3 activation by upregulating miR-302c-5p, thereby inhibiting Th17 cell differentiation.
Conclusions:
- KT2 alleviates UC by repressing Th17 cell differentiation.
- The mechanism involves the miR-302c-5p/STAT3 signaling axis.
- KT2 presents a potential therapeutic agent for ulcerative colitis.
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