Porcine reproductive and respiratory syndrome virus infection activates NOD2-RIP2 signal pathway in MARC-145 cells
Porcine reproductive and respiratory syndrome virus infection activates NOD2-RIP2 signal pathway in MARC-145 cells
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DOI：
10.1016/j.virol.2014.04.031
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发表时间：
2014-06-01
期刊：
影响因子：
3.7
通讯作者：
Xiao, Shaobo
中科院分区：
文献类型：
--
作者：
Jing, Huiyuan;Fang, Liurong;Xiao, Shaobo
核苷酸结合寡聚化结构域（NOD）样受体（NLRs）作为一组生殖系编码受体进化而来，检测细胞质病原体相关的分子模式。猪繁殖与呼吸综合征病毒（PRRSV）是一种严重危害全球养猪业的动脉病毒。通过检测10种NLRs的表达动力学，发现在prrsv感染的MARC-145细胞中，NOD2和NLRP3在感染后48 h内持续上调。进一步研究发现，PRRSV感染可增强RIP2的表达和磷酸化。通过siRNA敲低NOD2和RIP2可显著降低prrsv诱导的NF-kappa B亚基p65、JNK、Erk和p38 MAPK的磷酸化，以及IL-6、IL-8、tnf - α和RANTES在MARC-145细胞中的表达。此外，在prrsv攻击仔猪的肺泡巨噬细胞中，NOD2和RIP2 mRNA的表达在攻击后3、7和10 d均有所增加。总之，我们的研究结果表明，PRRSV感染激活NOD2-RIP2信号通路，诱导促炎反应。(C) 2014爱思唯尔公司版权所有。
Nucleotide-binding oligomerization domains (NOD)-like receptors (NLRs) evolve as a group of germline-encoded receptors that detect cytosolic pathogen-associated molecular patterns. Porcine reproductive and respiratory syndrome virus (PRRSV) is an Arterivirus that has been devastating the swine industry worldwide. By examining the expression kinetics of ten selected NLRs, NOD2 and NLRP3 were found to be continuously up-regulated in PRRSV-infected MARC-145 cells during 48 h of post-infection. Further study revealed that PRRSV infection enhanced the expression and phosphorylation of RIP2. Knockdown of NOD2 and RIP2 by siRNA significantly decreased PRRSV-induced phospholylation of NF-kappa B subunit p65, JNK, Erk and p38 MAPK, as well as the expression of IL-6, IL-8, TNF-alpha, and RANTES in MARC-145 cells. Moreover, increased expression of NOD2 and RIP2 mRNA were observed in alveolar macrophages isolated from PRRSV-challenged piglets at 3, 7 and 10 day post-challenge. Collectively, our results revealed that PRRSV infection activates NOD2-RIP2 signaling pathway to induce pro-inflammatory response. (C) 2014 Elsevier Inc. All rights reserved.