Respiratory syncytial virus infection of microglia exacerbates SH-SY5Y neuronal cell injury by inducing the secretion of inflammatory cytokines: A Transwell in vitro study.
Respiratory syncytial virus infection of microglia exacerbates SH-SY5Y neuronal cell injury by inducing the secretion of inflammatory cytokines: A Transwell in vitro study.
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呼吸道合胞病毒感染小胶质细胞通过诱导炎性细胞因子的分泌加重SH-SY5Y神经元细胞损伤:Transwell体外研究
DOI:
10.22038/ijbms.2020.49193.11263
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发表时间:
2021-03
影响因子:
2.2
通讯作者:
Huang SH
中科院分区:
文献类型:
--
作者:
Zhang XY;Zhang XC;Yu HY;Wang Y;Chen J;Wang Y;Yu L;Zhu GX;Cao XJ;Huang SH
To elucidate the mechanism of Respiratory Syncytial Virus (RSV) infection and central neuronal disease and to understand the role of microglia in neuronal injuries during RSV infection. The effects of RSV and the cytokines produced by RSV-infected CHME-5 microglial cells on SY5Y neuronal cells were evaluated based on an in vitro Transwell coculture system. Five treatment groups were established in this study, including the normal control SY5Y group, RSV+SY5Y infection group, (cytokine+CHME-5)+SY5Y Transwell group, (RSV+CHME-5)+SY5Y Transwell group, and (RSV+cytokine+CHME-5)+SY5Y Transwell group. The morphological and physical alterations in SY5Y cells and their synapses were analyzed by confocal microscopy. The mRNA and protein expression levels of TLR3/RIG-I, as well as the expression of Hv1, in microglia were measured by qRT-PCR and Western blot assays. In addition, the apoptosis ratio of neuronal cells was determined by flow cytometry. RSV infection activated the protein expression of Hv1 protein in microglia in vitro (P<0.05), induced morphological changes in SY5Y cells, lengthened synapses (73.36±0.12 μm vs 38.10±0.11 μm), simultaneously activated TLR3 and RIG-I protein expression (P<0.05), upregulated the secretion of the inflammatory cytokines TNF-α, IL-6, and IL-8 (P<0.01), and increased the apoptosis rate of SY5Y cells (P<0.01). The results demonstrate that RSV infection of microglia can induce SY5Y neuronal cell injury and stimulate apoptosis through inflammatory cytokine release.
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影响因子:
9
作者:
Bernardo, A. R.;Cosgaya, J. M.;Aranda, A.;Jimenez-Lara, A. M.
通讯作者:
Jimenez-Lara, A. M.
影响因子:
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McGavern DB
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影响因子:
2.2
作者:
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影响因子:
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作者:
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通讯作者:
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