Classical swine fever virus NS2 protein promotes interleukin-8 expression and inhibits MG132-induced apoptosis
Classical swine fever virus NS2 protein promotes interleukin-8 expression and inhibits MG132-induced apoptosis
复制标题
猪瘟病毒NS2蛋白促进白细胞介素8表达并抑制MG132诱导的细胞凋亡
DOI：
10.1007/s11262-011-0582-z
复制
发表时间：
2011-02
期刊：
影响因子：
1.6
通讯作者：
Wang, Jing
中科院分区：
文献类型：
--
作者：
Tang, Qinghai;Guo, Kangkang;Kang, Kai;Zhang, Yanming;He, Lei;Wang, Jing
猪瘟是由猪瘟病毒(CSFV)强毒株引起的猪出血性疾病，以弥漫性血管内凝血、血小板减少和免疫抑制为特征。到目前为止，CSFV产生的NS2蛋白在脑脊液发病机制中的作用尚不清楚。在这份报告中，我们通过检测CSFV NS2对促炎症CXC趋化因子、白介素8(IL-8)表达和细胞存活的影响来研究CSFV NS2的功能。建立了稳定表达CSFV NS2的猪脐静脉内皮细胞系(SUVEC)，结果表明，表达CSFV NS2的SUVEC细胞表达IL-8的水平比表达GFP的对照细胞、表达GFP-E2的细胞和未转染的细胞高约16倍。进一步的研究表明，CSFVNS2诱导内质网应激并激活核转录因子kappaB(NF-κB)，从而上调IL-8和抗凋亡蛋白Bcl2的表达。此外，表达GFPNS2的SUVEC细胞对MG132诱导的细胞凋亡具有抵抗力。提示CSFV NS2在炎症反应和持续性CSFV感染中起重要作用。这些发现为CSFV NS2的功能提供了新的信息。
Classical swine fever (CSF) caused by virulent strains of classical swine fever virus (CSFV) is a hemorrhagic disease of pigs and is characterized by disseminated intravascular coagulation, thrombocytopenia, and immunosuppression. Until now, the role of the NS2 protein produced by CSFV in the pathogenesis of CSF is not well understood. In this report, we investigated the function of CSFV NS2 by examining its effects on the pro-inflammatory CXC chemokine, interleukin-8 (IL-8) expression, and cell survival. Stable swine umbilical vein endothelial cell line (SUVEC) expressing CSFV NS2 were established and showed that CSFV NS2 expressing SUVEC cells express approximately 16-fold higher levels of IL-8 as compared to control vector GFP-expressing cells, GFP-E2 expressing cells, and untransfected cells. Further studies showed that CSFV NS2 induced endoplasmic reticulum stress and activated the nuclear transcription factor kappa B (NF-κB), which is responsible for the up-regulation of IL-8 and the anti-apoptotic protein, Bcl-2, expression. In addition, the GFPNS2-expressing SUVEC cells were resistant to MG132-induced apoptosis. This study suggested that CSFV NS2 plays an important role in the inflammatory response and in persistent CSFV infection. These findings provide novel information on the function of the poorly characterized CSFV NS2.
登录
查看更多内容
影响因子：
100.3
作者：
Qiutang Li;I. Verma
通讯作者：
Qiutang Li;I. Verma
影响因子：
4.8
作者：
Laitusis, AL;Brostrom, MA;Brostrom, CO
通讯作者：
Brostrom, CO
影响因子：
3.8
作者：
Doceul, Virginie;Charleston, Bryan;Seago, Julian
通讯作者：
Seago, Julian
影响因子：
5.4
作者：
Moser, C;Stettler, P;Hofmann, MA
通讯作者：
Hofmann, MA
影响因子：
0.8
作者：
Alejandro Núñez;J. C. Gómez-Villamandos;P. Sánchez-Cordón;M. F. D. Marco;M. Pedrera;Francisco J. Salguero;Librado Carrasco
通讯作者：
Alejandro Núñez;J. C. Gómez-Villamandos;P. Sánchez-Cordón;M. F. D. Marco;M. Pedrera;Francisco J. Salguero;Librado Carrasco