Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/70561
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dc.contributor.authorChen, C.J.en_US
dc.contributor.authorChen, J.H.en_US
dc.contributor.authorChen, S.Y.en_US
dc.contributor.authorLiao, S.L.en_US
dc.contributor.authorRaung, S.L.en_US
dc.date2004zh_TW
dc.date.accessioned2014-06-11T06:00:00Z-
dc.date.available2014-06-11T06:00:00Z-
dc.identifier.issn0022-538Xzh_TW
dc.identifier.urihttp://hdl.handle.net/11455/70561-
dc.description.abstractInfection with Japanese encephalitis virus (JEV) causes cerebral inflammation and stimulates inflammatory cytokine expression. Glial cells orchestrate immunocyte recruitment to focal sites of viral infection within the central nervous system (CNS) and synchronize immune cell functions through a regulated network of cytokines and chemokines. Since immune cell infiltration is prominent, we investigated the production of a responding chemoattractant, RANTES (regulated upon activation, normal T-cell expressed and secreted), in response to JEV infection of glial cells: Infection with JEV was found to elicit the production of RANTES from primary neurons/glia, mixed glia, microglia, and astrocytes but not from neuron cultures. The production of RANTES did not seem to be directly responsible for JEV-induced neuronal death but instead contributed to the recruitment of immune cells. RANTES expression required viral replication and the activation of extracellular signal-regulated kinase (ERK) as well as transcription factors, including nuclear factor kappa B (NF-kappaB) and nuclear factor IL-6 (NF-IL-6). The induction of RANTES expression by JEV infection in glial cells needed the coordinate activation of NF-kappaB and NF-IL-6. Using enzymatic inhibitors, we demonstrated a strong correlation between the ERK signaling pathway and RANTES expression. However, JEV replication was not dependent on the activation of ERK, NF-kappaB, and NF-IL-6. Altogether, these results demonstrated that infection of glial cells by JEV provided the early ERK-, NF-kappaB-, and NF-IL-6-mediated signals that directly activated RANTES expression, which might be involved in the initiation and amplification of inflammatory responses in the CNS.en_US
dc.language.isoen_USzh_TW
dc.relationJournal of Virologyen_US
dc.relation.ispartofseriesJournal of Virology, Volume 78, Issue 22, Page(s) 12107-12119.en_US
dc.relation.urihttp://dx.doi.org/10.1128/jvi.78.22.12107-12119.2004en_US
dc.subjectnf-kappa-ben_US
dc.subjectcentral-nervous-systemen_US
dc.subjecttumor-necrosis-factoren_US
dc.subjectblood-brain-barrieren_US
dc.subjectmonocyte chemoattractant protein-1en_US
dc.subjectfelineen_US
dc.subjectimmunodeficiency virusen_US
dc.subjectrespiratory syncytial virusen_US
dc.subjectairwayen_US
dc.subjectepithelial-cellsen_US
dc.subjectnitric-oxide synthaseen_US
dc.subjectlymphocytic choriomeningitisen_US
dc.titleUpregulation of RANTES gene expression in neuroglia by Japanese encephalitis virus infectionen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1128/jvi.78.22.12107-12119.2004zh_TW
item.cerifentitytypePublications-
item.grantfulltextnone-
item.languageiso639-1en_US-
item.fulltextno fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
Appears in Collections:期刊論文
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