Transmissible gastroenteritis virus infection induces NF-κB activation through RLR-mediated signaling.
Transmissible gastroenteritis virus infection induces NF-κB activation through RLR-mediated signaling.
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DOI：
10.1016/j.virol.2017.04.024
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发表时间：
2017-07
期刊：
影响因子：
3.7
通讯作者：
Fang L
中科院分区：
文献类型：
--
作者：
Ding Z;An K;Xie L;Wu W;Zhang R;Wang D;Fang Y;Chen H;Xiao S;Fang L
猪传染性胃肠炎病毒（TGEV）是一种引起仔猪严重腹泻的猪肠道冠状病毒。TGEV的发病机制与炎症密切相关。在本研究中，我们发现TGEV感染以时间和剂量依赖的方式激活猪肾细胞中的转录因子NF-κB、IRF 3和AP-1。用NF-κ B特异性抑制剂BAY 11 -7082处理显著降低TGEV诱导的促炎细胞因子产生，但不影响病毒复制。在敲低视黄酸诱导基因I（RIG-I）样受体（RLR）或其衔接子MAVS和STING后，NF-κB亚基p65的磷酸化和促炎细胞因子的产生大大减少，而在Toll样受体衔接子MyD 88和TRIF沉默后，仅观察到细胞中NF-κB亚基p65的磷酸化和促炎细胞因子的产生轻微减少。此外，TGEV感染显著上调RIG-I和MDA 5的mRNA表达。总之，我们的结果表明，RLR信号通路参与TGEV诱导的炎症反应。传染性胃肠炎病毒（TGEV）感染激活NF-κB。抑制NF-κB活化不影响TGEV的复制。RLR信号通路参与TGEV诱导的炎症反应。TGEV感染显著上调RIG-I和MDA 5的mRNA表达。
Transmissible gastroenteritis virus (TGEV) is a porcine enteric coronavirus which causes lethal severe watery diarrhea in piglets. The pathogenesis of TGEV is strongly associated with inflammation. In this study, we found that TGEV infection activates transcription factors NF-κB, IRF3 and AP-1 in a time- and dose-dependent manner in porcine kidney cells. Treatment with the NF-κB-specific inhibitor BAY11-7082 significantly decreased TGEV-induced proinflammatory cytokine production, but did not affect virus replication. Phosphorylation of NF-κB subunit p65 and proinflammatory cytokine production were greatly decreased after knockdown of retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) or its adaptors MAVS and STING, while only slight reduction was observed in cells following silencing of Toll-like receptor adaptors, MyD88 and TRIF. Furthermore, TGEV infection significantly upregulated mRNA expression of RIG-I and MDA5. Taken together, our results indicate that the RLR signaling pathway is involved in TGEV-induced inflammatory responses. Transmissible gastroenteritis virus (TGEV) infection activates NF-κB. Inhibition of NF-κB activation does not affect TGEV replication. RLR signaling pathway is involved in TGEV-induced inflammatory responses. TGEV infection significantly upregulates mRNA expression of RIG-I and MDA5.
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