期刊
ARCHIVES OF VIROLOGY
卷 162, 期 6, 页码 1495-1505出版社
SPRINGER WIEN
DOI: 10.1007/s00705-017-3226-3
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资金
- First Affiliated Hospital [ST-2014-017]
Increasing evidence confirms the involvement of virus infection and miRNA, such as miR-146a, in neuroinflammation-associated epilepsy. In the present study, we investigated the upregulation of miR-146a with RT-qPCR and in situ hybridization methods in a mice infection model of Japanese encephalitis virus (JEV) and in vitro. Subsequently we investigated the involvement of miR-146a in modulating JEV-induced neuroinflammation. It was demonstrated that JEV infection promoted miR-146a production in BALB/c mice brain and in cultured mouse microglial C8-B4 cells, along with pro-inflammatory cytokines, such as IL-1 beta, IL-6, TNF-alpha, IFN-beta and IFN-alpha. We also found that miR-146a exerted negative regulatory effects upon IL-1 beta, IL-6, TNF-alpha, IFN-beta and IFN-alpha in C8-B4 cells. Accordingly, miR-146a downregulation with a miR-146a inhibitor promoted the upregulation of IL-1 beta, IL-6, TNF-alpha, IFN-beta and IFN-alpha, whereas miR-146a upregulation with miR-146a mimics reduced the upregulation of these cytokines. Moreover, miR-146a exerted no regulation upon JEV growth in C8-B4 cells. In conclusion, JEV infection upregulated miR-146a and pro-inflammatory cytokine production, in mice brain and in cultured C8-B4 cells. Furthermore, miR-146a negatively regulated the production of JEV-induced pro-inflammatory cytokines, in virus growth independent fashion, identifying miR-146a as a negative feedback regulator in JEV-induced neuroinflammation, and possibly in epilepsy.
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