title: Astrocytic alteration induced by Japanese encephalitis virus infection.
abstract: The neurotropism of Japanese encephalitis virus (EV) has not been well characterized. Astrocytes are parts of the blood-brain barrier, a major source of chemokines, and critical effectors of central inflammation. Thus, astrocytes might play some role as JEV travels from the peripheral to the CNS and/or the resultant encephalitis. Using rat cortical cultures, we found that JEV can cause cellular and/or functional changes in astrocytes as indicated by increased expression of interleukin-6 (IL-6), regulated by activation, normal T cell expressed and secreted (RANTES), and monocyte chemotactic protein 1 (MCP-1), increased lactate release and glucose uptake, and attenuation of glutamate toxicity. These modulations occur needed by the cells for compensation and may affect neuron and/or astrocyte function.
authors.affiliation: Department of Education and Research, Taichung Veterans General Hospital, Taiwan, ROC.
authors.forename: C J
authors.initials: CJ
authors.lastname: Chen
authors.forename: S L
authors.initials: SL
authors.lastname: Liao
authors.forename: M D
authors.initials: MD
authors.lastname: Kuo
authors.forename: Y M
authors.initials: YM
authors.lastname: Wang
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D018920:Coculture Techniques; D016207:Cytokines / Q000378:metabolism; D004664:Encephalitis Virus, Japanese; D004672:Encephalitis, Japanese / Q000378:metabolism / Q000473:pathology*; D018698:Glutamic Acid / Q000506:poisoning; D009474:Neurons / Q000473:pathology; D009498:Neurotoxins / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D016207:Cytokines; D009498:Neurotoxins; D018698:Glutamic Acid