Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/69986
標題: Glial activation involvement in neuronal death by Japanese encephalitis virus infection
作者: Chen, C.J.
Ou, Y.C.
Lin, S.Y.
Raung, S.L.
Liao, S.L.
Lai, C.Y.
Chen, S.Y.
Chen, J.H.
關鍵字: microglial activation
tyrosine kinase
nervous-system
in-vitro
astrocytes
induction
cytokines
disease
cell
neuroinflammation
期刊/報告no:: Journal of General Virology, Volume 91, Page(s) 1028-1037.
摘要: Japanese encephalitis is characterized by profound neuronal destruction/dysfunction and concomitant microgliosis/astrogliosis. Although substantial activation of glia is observed in Japanese encephalitis virus (JEV)-induced Japanese encephalitis, the inflammatory responses and consequences of astrocytes and microglial activation after JEV infection are not fully understood. In this study, infection of cultured neurons/glia with JEV caused neuronal death and glial activation, as evidenced by morphological transformation, increased cell proliferation and elevated tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-6 and RANTES (regulated upon activation, normal T-cell expressed and secreted) production. Replication-competent JEV caused all glial responses and neurotoxicity. However, replication-incompetent JEV lost these abilities, except for the ability to change microglial morphology. The bystander damage caused by activated glia also contributed to JEV-associated neurotoxicity. Microglia underwent morphological changes, increased cell proliferation and elevated TNF-alpha, IL-1 beta, IL-6 and RANTES expression in response to JEV infection. In contrast, IL-6 and RANTES expression, but no apparent morphological changes, proliferation or TNF-alpha/IL-1 beta expression, was demonstrated in JEV-infected astrocytes. Supernatants of JEV-infected microglia, but not JEV-infected astrocytes, induced glial activation and triggered neuronal death. Antibody neutralization studies revealed that TNF-alpha and IL-1 beta, but not RANTES or IL-6, released by activated microglia appeared to play roles in JEV-associated neurotoxicity. In conclusion, following JEV infection, neuronal death was accompanied by concomitant microgliosis and astrogliosis, and neurotoxic mediators released by JEV-activated microglia, rather than by JEV-activated astrocytes, had the ability to amplify the microglial response and cause neuronal death.
URI: http://hdl.handle.net/11455/69986
ISSN: 0022-1317
文章連結: http://dx.doi.org/10.1099/vir.0.013565-0
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