Astrocytic alteration induced by Japanese encephalitis virus infection.
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.
Chen
C J
CJ
Department of Education and Research, Taichung Veterans General Hospital, Taiwan, ROC.
Liao
S L
SL
Kuo
M D
MD
Wang
Y M
YM
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
D016207:Cytokines; D009498:Neurotoxins; D018698:Glutamic Acid