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PLAC8 通过干扰新生鼠 Th 细胞相关细胞因子释放促进 EV71 感染性炎症损伤。

PLAC8 promotes EV71 infected inflammatory lesion by disturbing Th-cell-related cytokines release in neonatal mouse.

机构信息

Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, 441053, China.

School of Basic Medicine, Hubei University of Arts and Science, Xiangyang, 441053, China.

出版信息

Virology. 2021 Dec;564:39-45. doi: 10.1016/j.virol.2021.10.001. Epub 2021 Oct 8.

Abstract

Enterovirus 71 can cause severe hand, foot, and mouth disease (HFMD) in children. However, little is known about the mechanism of inflammatory disorders caused by EV71 infection and why severe cases are mainly children aged under-three. In current study, using mRNA microarray assay, the differential expression of Placenta-specific 8 (PLAC8) was identified in mice brain. In addition, we found that PLAC8 expression was down-regulated with age in mice lung tissues and human peripheral blood. Then, we further proved that PLAC8 could promote inflammation progress and disturb Th1/Th2/Th17/Treg related cytokines release after EV71 infection using PLAC8 plasmid over-expressed neonatal mouse model. Our data suggest that PLAC8 might play a crucial role in Th cell differentiation and inflammatory damage caused by EV71 infection in infants. Thus, our findings would help understand the causes of severe inflammatory injury in infants during EV71 infection, and provide new insights into the prevention and control of severe HFMD.

摘要

肠道病毒 71 型可引起儿童重症手足口病(HFMD)。然而,人们对 EV71 感染引起炎症性疾病的机制以及为什么重症病例主要是三岁以下儿童知之甚少。在本研究中,我们使用 mRNA 微阵列分析鉴定了小鼠脑中胎盘特异性 8(PLAC8)的差异表达。此外,我们发现 PLAC8 在小鼠肺组织和人外周血中的表达随年龄增长而下调。然后,我们使用 PLAC8 质粒过表达新生小鼠模型进一步证明,PLAC8 可促进 EV71 感染后炎症的进展,并干扰 Th1/Th2/Th17/Treg 相关细胞因子的释放。我们的数据表明,PLAC8 可能在 EV71 感染引起的婴儿 Th 细胞分化和炎症损伤中发挥关键作用。因此,我们的研究结果将有助于了解 EV71 感染期间婴儿严重炎症损伤的原因,并为重症 HFMD 的预防和控制提供新的思路。

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