畜牧兽医学报 ›› 2021, Vol. 52 ›› Issue (2): 450-459.doi: 10.11843/j.issn.0366-6964.2021.02.017

• 预防兽医 • 上一篇    下一篇

程序性细胞死亡因子10抑制Ⅰ型干扰素表达并促进FMDV复制

曾宗波1,2, 马旭升2, 罗志宽2, 齐亚银1*, 郑海学2*   

  1. 1. 石河子大学动物科技学院, 石河子 832000;
    2. 中国农业科学院兰州兽医研究所, 家畜疫病病原学国家重点实验室, 兰州 730046
  • 收稿日期:2020-07-13 出版日期:2021-02-23 发布日期:2021-02-24
  • 通讯作者: 齐亚银,主要从事动物传染病诊断与防治研究,E-mail:qiyayin@163.com;郑海学,主要从事动物传染病与流行病学研究,Tel:0931-8342086,E-mail:haixuezheng@163.com
  • 作者简介:曾宗波(1995-),男,四川三台人,硕士生,主要从事动物传染病诊断与防制研究,E-mail:904588641@qq.com
  • 基金资助:
    国家自然科学基金(31760737)

Programmed Cell Death Factor 10 Inhibits Type Ⅰ Interferon Expression and Promotes the Replication of Foot-and-mouth Disease Virus

ZENG Zongbo1,2, MA Xusheng2, LUO Zhikuan2, QI Yayin1*, ZHENG Haixue2*   

  1. 1. College of Animal Science and Technology, Shihezi University, Shihezi 832000, China;
    2. State Key Laboratory of Veterinary Etiological Biology, National Foot-and-Mouth Disease Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, China
  • Received:2020-07-13 Online:2021-02-23 Published:2021-02-24

摘要: 旨在探究宿主蛋白程序性细胞死亡因子10(programmed cell death factor 10,PDCD10)通过抑制Ⅰ型干扰素表达进而促进口蹄疫病毒(foot-and-mouth disease virus,FMDV)的复制。首先,本研究验证了过表达和沉默PDCD10对FMDV复制的影响,接着利用双荧光素酶报告系统探究PDCD10对Ⅰ型干扰素信号通路活化的影响,最后,利用实时荧光定量PCR探究PDCD10对Ⅰ型干扰素通路下游刺激基因(IFN-stimulated genes,ISGs)转录的影响。结果表明,过表达PDCD10显著促进FMDV的复制,沉默PDCD10显著抑制FMDV的复制。与对照相比,过表达PDCD10后感染仙台病毒(Sendai virus,SeV)的细胞培养液上清液显著促进FMDV复制,进一步,PDCD10显著抑制SeV诱导的IFN-β启动子以及NF-κB的激活且呈剂量依赖性,并且PDCD10负调控Ⅰ型干扰素通路信号分子转录,最后还发现PDCD10负调控Ⅰ型干扰素下游ISGs转录。本研究结果为深入探究PDCD10在抗病毒天然免疫中的作用积累了资料。

关键词: 程序性细胞死亡因子10, PDCD10, FMDV, Ⅰ型干扰素信号通路, IFN-β

Abstract: The purpose of this study is to explore how the host protein programmed cell death factor 10 (PDCD10) can inhibit the expression of type Ⅰ interferon to promote the replication of foot-and-mouth disease virus (FMDV). First, this study verified the effect of overexpression and silencing of PDCD10 on FMDV replication. Secondly, the dual-luciferase reporter system was used to explore the effect of PDCD10 on the activation of type Ⅰ interferon signaling pathway. Finally, real-time fluorescent quantitative PCR was used to explore the effect of PDCD10 on the transcription of stimulating genes downstream of the type Ⅰ interferon pathway. The results showed that overexpression of PDCD10 significantly promoted FMDV replication while silencing PDCD10 significantly inhibited FMDV replication. Compared with the control, the cell culture supernatant infected with Sendai virus (SeV) after overexpression of PDCD10 significantly promoted FMDV replication. Furthermore, PDCD10 significantly inhibited the activation of IFN-β promoter and NF-κB induced by SeV in a dose-dependent manner, and PDCD10 negatively regulated the transcription of type Ⅰ interferon pathway signal molecules. Finally, it was found that PDCD10 negatively regulated the transcription of ISGs downstream of type Ⅰ interferon. The results of this study have accumulated data for the in-depth exploration of the role of PDCD10 in antiviral innate immunity.

Key words: programmed cell death factor 10, PDCD10, FMDV, Type Ⅰ interferon signaling pathway, IFN-β

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