Porcine deltacoronavirus E protein induces interleukin-8 production via NF-xB and AP-1 activation

文献类型： 外文期刊

第一作者： Wu, Yang

作者： Wu, Yang;Shi, Zhaorong;Chen, Jianfei;Zhang, Hongling;Li, Mingwei;Zhao, Ying;Shi, Hongyan;Shi, Da;Guo, Longjun;Feng, Li

作者机构：

关键词： PDCoV; IL-8; Inflammation; E

期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.246； 五年影响因子：3.565 ）

ISSN： 0378-1135

年卷期： 2022 年 274 卷

页码：

收录情况： SCI

摘要： Infection induces the production of proinflammatory cytokines and chemokines such as interleukin-8 (IL-8) and interleukin-6 (IL-6). Although they facilitate local antiviral immunity, their excessive release leads to life -threatening cytokine release syndrome, exemplified by the severe cases of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In the present study, we found that interleukin-8 (IL-8) was upregulated by PDCoV infection. We then demonstrated that PDCoV E protein induced IL-8 production and that the TM domain and the C-terminal domain of the E protein were important for IL-8 production. Subsequently, we showed here that deleting the AP-1 and NF-xB binding motif in porcine IL-8 promoter abrogated its activation, suggesting that IL-8 expression was dependent on AP-1 and NF-xB. Further-more, PDCoV E induced IL-8 production, which was also dependent on the NF-xB pathway through activating nuclear factor p65 phosphorylation and NF-xB inhibitor alpha (IxBa) protein phosphorylation, as well as inducing the nuclear translocation of p65, eventually resulting in the promotion of IL-8 production. PDCoV E also activated c-fos and c-jun, both of which are members of the AP-1 family. These findings provide new insights into the molecular mechanisms of PDCoV-induced IL-8 production and help us further understand the pathogenesis of PDCoV infection.

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