Expression Pattern Analysis of Antiviral Genes and Inflammatory Cytokines in PEDV-Infected Porcine Intestinal Epithelial Cells
Expression Pattern Analysis of Antiviral Genes and Inflammatory Cytokines in PEDV-Infected Porcine Intestinal Epithelial Cells
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PEDV感染猪肠上皮细胞抗病毒基因和炎症细胞因子的表达模式分析
DOI：
10.3389/fvets.2020.00075
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发表时间：
2020-02-18
影响因子：
3.2
通讯作者：
Bao, Wenbin
中科院分区：
文献类型：
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作者：
Wang, Shiqin;Wu, Jiayun;Bao, Wenbin
由猪流行性腹泻病毒（PEDV）感染引起的新生儿和哺乳仔猪腹泻病是全球养猪业经济损失的主要原因。在这项研究中，我们探讨了宿主先天免疫应答PEDV感染的分子机制。分析PEDV刺激猪小肠上皮（IPEC-J2）细胞后抗病毒基因RIG-1、PKR、OAS1、Mx1、Mx2和炎症因子IFN-α、IFN-β、TNF-α、IL-6、IL-8、IL-12的表达动态。结果显示，感染后0 ~ 4 h内，抗病毒基因（PKR、OAS1、Mx2）和炎症因子（IFN-α、TNF-α）的表达显著降低（P < 0.05）。然而，在12 ~ 24 h，所有抗病毒基因和炎症因子均上调（P < 0.05），并在此期间观察到细胞病变。RIG-1、PKR、OAS1、Mx1、Mx2的表达在整个感染过程中呈显著正相关（P < 0.01）。结果提示RIG-1、PKR、OAS1、Mx1和Mx2基因可能在仔猪PEDV感染中起重要作用。最初，PEDV通过抑制IFN-α转录和干扰PKR、OAS1和Mx2的抗病毒功能表现出细胞侵袭性，最终诱导强烈的炎症反应。在细胞水平上研究抗病毒基因和炎症因子与PEDV感染的关系，为研究仔猪对PEDV感染的抗性机制提供参考。
Porcine diarrhea disease in newborn and suckling piglets due to infection with porcine epidemic diarrhea virus (PEDV) is a leading cause of economic loss in the pig industry globally. In this study, we investigated the molecular mechanism of the host innate immune response to PEDV infection. The expression dynamics of antiviral genes (e.g., RIG-1, PKR, OAS1, Mx1, and Mx2) and inflammatory cytokines (e.g., IFN-α, IFN-β, TNF-α, IL-6, IL-8, and IL-12) in porcine small intestinal epithelial (IPEC-J2) cells were analyzed following PEDV stimulation. The results showed that the expression of antiviral genes (e.g., PKR, OAS1, and Mx2) and inflammatory cytokines (e.g., IFN-α and TNF-α) were significantly reduced within 0–4 h post-infection (P < 0.05). However, all antiviral genes and inflammatory cytokines were up-regulated from 12 to 24 h (P < 0.05), and cytopathic changes were observed during this time. The expression of RIG-1, PKR, OAS1, Mx1, and Mx2 were significantly and positively correlated to each other during the entire infection (P < 0.01). The results suggested that the RIG-1, PKR, OAS1, Mx1, and Mx2 genes may play an important role in PEDV infection in piglets. Initially, PEDV displayed cellular invasion by inhibiting IFN-α transcription and interfering with the antiviral function of PKR, OAS1, and Mx2, ultimately induced an intense inflammatory response. The relationship between antiviral genes and inflammatory cytokines with PEDV infection at the cellular level provides a reference for studying the mechanism of resistance to PEDV infection in piglets.