MiR-146a down-regulates inflammatory response by targeting TLR3 and TRAF6 in Coxsackievirus B infection
- Yanru Fei1,
- Anita Chaulagain1,
- Tianying Wang1,
- Yang Chen1,
- Jinchang Liu2,
- Ming Yi1,
- Ying Wang1,
- Yike Huang3,
- Lexun Lin1,
- Sijia Chen1,
- Weizhen Xu1,
- Lei Tong1,
- Xiaoyu Wu4,
- Dechao Zhao4,
- Fengmin Zhang5,
- Wenran Zhao3 and
- Zhaohua Zhong1,6
- 1 Department of Microbiology, Harbin Medical University;
- 2 Harbin Medical University Department of Microbiology;
- 3 Department of Cell Biology, Harbin Medical University;
- 4 Department of Cardiology, The First Hospital of Harbin Medical University;
- 5 Department of Micriobilogy, Harbin Medical University
- ↵* Corresponding author; email: zhongzh{at}hrbmu.edu.cn
Abstract
Coxsackievirus B (CVB) is the major cause of human myocarditis and dilated cardiomyopathy. Toll-like receptor 3 (TLR3) is an intracellular sensor to detect pathogen’s dsRNA. TLR3, along with TRAF6, triggers inflammatory response through NF-κB signaling pathway. In the cells infected with CVB type 3 (CVB3), the abundance of miR-146a was significantly increased. The role of miR-146a in CVB infection is unclear. In this study, TLR3 and TRAF6 were identified as the targets of miR-146a. The elevated miR-146a inhibited NF-κB translocation and subsequently down-regulated proinflammatory cytokine expression in the CVB3-infected cells. Therefore, the NF-κB pathway can be doubly blocked by miR-146a through targeting of TLR3 and TRAF6. MiR-146a may be a negative regulator on inflammatory response and an intrinsic protective factor in CVB infection.
Keywords
- Received May 20, 2019.
- Accepted October 28, 2019.
- Published by Cold Spring Harbor Laboratory Press for the RNA Society
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