Classical Swine Fever Virus Infection and Its NS4A Protein Expression Induce IL-8 Production through MAVS Signaling Pathway in Swine Umbilical Vein Endothelial Cells.
Classical Swine Fever Virus Infection and Its NS4A Protein Expression Induce IL-8 Production through MAVS Signaling Pathway in Swine Umbilical Vein Endothelial Cells.
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DOI：
10.3389/fmicb.2017.02687
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发表时间：
2017
影响因子：
5.2
通讯作者：
Zhang Y
中科院分区：
文献类型：
--
作者：
Dong W;Lv H;Guo K;Wang T;Ouyang Y;Jin M;Zhang Y
猪瘟病毒(CSFV)感染猪引起以出血、弥漫性血管内凝血和白细胞减少为特征的严重疾病。IL-8是中性粒细胞的主要趋化因子和激活剂，调节内皮细胞的通透性，可能与CSFV感染后出血有关。到目前为止，IL-8在CSFV感染过程中调节的分子机制还不是很清楚。在这里，我们发现CSFV感染诱导了IL-8的产生，而IL-8的上调需要病毒在猪脐静脉内皮细胞(SUVECs)中复制。此外，在CSFV感染后，MAVS的表达增加，并且是产生IL-8所必需的。此外，ROS参与了CSFV诱导的IL-8的产生。随后的研究表明，ROS参与了MAVS诱导的IL-8的产生，CSFV通过MAVS途径诱导产生ROS。这些结果表明CSFV通过MAVS途径和ROS的产生来诱导IL-8的产生。NS4A在CSFV发病机制中的作用尚不清楚。在本研究中，我们进一步证明CSFV NS4A通过增强MAVS途径诱导IL-8的产生并促进CSFV的复制。此外，我们还发现CSFV NS4A定位于胞核和细胞质，包括内质网和线粒体。综上所述，这些结果为深入研究CSFV感染过程中IL-8的调节机制和NS4A的作用提供了新的思路。
Classical swine fever virus (CSFV) infection causes a severe disease of pigs, which is characterized by hemorrhage, disseminated intravascular coagulation, and leucopenia. IL-8, a main chemokine and activator of neutrophils, regulates the permeability of endothelium, which may be related to the hemorrhage upon CSFV infection. Until now, the molecular mechanisms of IL-8 regulation during CSFV infection are poorly defined. Here, we showed that CSFV infection induced IL-8 production and the upregulation of IL-8 required virus replication in swine umbilical vein endothelial cells (SUVECs). Additionally, MAVS expression was increased and was required for IL-8 production upon CSFV infection. Moreover, ROS was involved in CSFV-induced IL-8 production. Subsequent studies demonstrated that ROS was involved in MAVS-induced IL-8 production and CSFV induced ROS production through MAVS pathway. These results indicate that CSFV induces IL-8 production through MAVS pathway and production of ROS. The role of NS4A in the pathogenesis of CSFV is not well-understood. In this study, we further demonstrated that CSFV NS4A induced IL-8 production through enhancing MAVS pathway and promoted CSFV replication. In addition, we discovered that CSFV NS4A was localized in the cell nucleus and cytoplasm, including endoplasmic reticulum (ER) and mitochondria. Taken together, these results provide insights into the mechanisms of IL-8 regulation and NS4A functions during CSFV infection.
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影响因子：
4.6
作者：
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