Influenza Virus Induces Inflammatory Response in Mouse Primary Cortical Neurons with Limited Viral Replication.
Influenza Virus Induces Inflammatory Response in Mouse Primary Cortical Neurons with Limited Viral Replication.
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流感病毒在小鼠原代皮质神经元中诱导炎症反应，病毒复制有限
DOI：
10.1155/2016/8076989
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发表时间：
2016
影响因子：
--
通讯作者：
Li K
中科院分区：
文献类型：
--
作者：
Wang G;Li R;Jiang Z;Gu L;Chen Y;Dai J;Li K
与常规的嗜神经病毒不同，甲型流感病毒已在人类和动物模型的脑组织中检测到。为了研究神经元与甲型流感病毒之间的相互作用，分离小鼠皮层神经元，感染人H1N1流感病毒，然后检查参与免疫应答的各种炎症分子的产生。我们发现流感病毒在神经元中的复制是有限的，尽管早期的病毒转录没有受到影响。病毒诱导的神经元存活率在感染后6 h（p.i.）但在感染后24小时增加。这取决于病毒株。病毒诱导的原代皮层神经元凋亡和细胞病变在感染后24 h不明显。在感染后6 h和24 h，炎性细胞因子、趋化因子和I型干扰素的mRNA水平上调。这些结果表明，流感病毒在小鼠原代皮层神经元中诱导炎症反应，但病毒复制有限。病毒感染诱导的神经炎症中释放的细胞因子可能在流感脑病中起关键作用，而不是在病毒复制诱导的细胞病变中。
Unlike stereotypical neurotropic viruses, influenza A viruses have been detected in the brain tissues of human and animal models. To investigate the interaction between neurons and influenza A viruses, mouse cortical neurons were isolated, infected with human H1N1 influenza virus, and then examined for the production of various inflammatory molecules involved in immune response. We found that replication of the influenza virus in neurons was limited, although early viral transcription was not affected. Virus-induced neuron viability decreased at 6 h postinfection (p.i.) but increased at 24 h p.i. depending upon the viral strain. Virus-induced apoptosis and cytopathy in primary cortical neurons were not apparent at 24 h p.i. The mRNA levels of inflammatory cytokines, chemokines, and type I interferons were upregulated at 6 h and 24 h p.i. These results indicate that the influenza virus induces inflammatory response in mouse primary cortical neurons with limited viral replication. The cytokines released in viral infection-induced neuroinflammation might play critical roles in influenza encephalopathy, rather than in viral replication-induced cytopathy.