[Proinflammatory Cytokine and Chemokine Production of Mouse Macrophages in Response to EV-A71 Infection].

Guangcheng Xie, Nijun Guo, Ying Wang, Yongkang Zhou, Dandi Li, Miao Jin, Lili Pang, Xiaoman Sun, Qing Zhang, Zhaojun Duan
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Abstract

To study the replication and antiviral innate immunity of EV-A71 in mouse macrophages, we selected the mouse macrophage RAW264.7cell line as a model. An absolute quantitative PCR detection method was constructed to detect the viral load of EV-A71 in RAW264.7cells.RT-qPCR detected the fold changes of the proinflammatory cytokine, chemokine, and pattern recognition receptors at different time points post-infection in RAW264.7cells infected with EV-A71 and UV-inactivated EV-A71.The results revealed that the viral load of EV-A71 in RAW264.7cells decreased as the time post-infection increased. Proinflammatory cytokines, including IL-1β,IL-6,TNF-α,and chemokines, including IP-10,MCP-1,and MIP-1αwere induced, and the mRNA expression levels of TLR2,TLR1,TLR6,MDA5,and RIG-I were up-regulated. These results indicate that EV-A71 could replicate in mouse macrophages at a lower level, and proinflammatory cytokine and chemokine responses were induced.

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小鼠巨噬细胞对EV-A71感染的促炎细胞因子和趋化因子产生[j]。
为了研究EV-A71在小鼠巨噬细胞中的复制和抗病毒先天免疫,我们选择小鼠巨噬细胞raw264.7细胞系作为模型。构建绝对定量PCR检测方法检测raw264.7细胞中EV-A71病毒载量。RT-qPCR检测EV-A71和uv灭活EV-A71感染raw264.7细胞后不同时间点促炎细胞因子、趋化因子和模式识别受体的折叠变化。结果显示,随着感染后时间的延长,raw264.7细胞中EV-A71病毒载量降低。诱导IL-1β、IL-6、TNF-α等促炎因子和IP-10、MCP-1、mip -1α等趋化因子表达,上调TLR2、TLR1、TLR6、MDA5、rig -1 mRNA表达水平。上述结果表明,EV-A71能够在小鼠巨噬细胞中低水平复制,并诱导促炎细胞因子和趋化因子反应。
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