期刊
VETERINARY RESEARCH
卷 48, 期 -, 页码 -出版社
BIOMED CENTRAL LTD
DOI: 10.1186/s13567-017-0450-5
关键词
-
资金
- National Key Research and Development Program of China [2016YFD0500704, 2016YFD0500900]
- Chinese National Science Foundation [31472172]
- Priority Academic Program Development of Jiangsu Higher Education Institution (PAPD)
- Priority Academic Program Development of Jiangsu Higher Education Institution (TAPP)
Bovine herpesvirus 1 (BoHV-1) infection enhanced the generation of inflammatory mediator reactive oxidative species (ROS) and stimulated MAPK signaling that are highly possibly related to virus induced inflammation. In this study, for the first time we show that BoHV-1 infection manipulated phospholipase C (PLC) signaling, as demonstrated by the activation of PLC gamma-1 at both early stages [at 0.5 h post-infection (hpi)] and late stages (4-12 hpi) during the virus infection of MDBK cells. Viral entry, and de novo protein expression and/or DNA replication were potentially responsible for the activation of PLC gamma-1 signaling. PLC signaling inhibitors of both U73122 and edelfosine significantly inhibited BoHV-1 replication in both bovine kidney cells (MDBK) and rabbit skin cells (RS-1) in a dose-dependent manner by affecting the virus entry stage(s). In addition, the activation of Erk1/2 and p38MAPK signaling, and the enhanced generation of ROS by BoHV-1 infection were obviously ameliorated by chemical inhibition of PLC signaling, implying the requirement of PLC signaling in ROS production and these MAPK pathway activation. These results suggest that the activation of PLC signaling is a potential pathogenic mechanism for BoHV-1 infection.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据