Japanese encephalitis virus infection decrease endogenous IL-10 production: Correlation with microglial activation and neuronal death

Japanese encephalitis virus infection decrease endogenous IL-10 production: Correlation with... The anti-inflammatory cytokine interleukin (IL)-10 is synthesized in the central nervous system (CNS) and acts to limit clinical symptoms of stroke, multiple sclerosis, Alzheimer's disease, meningitis, and the behavioral changes that occur during bacterial infections. Expression of IL-10 is critical during the course of most major diseases in the CNS and promotes survival of neurons and all glial cells in the brain by blocking the effects of proinflammatory cytokines and by promoting expression of cell survival signals. In order to assess functional importance of this cytokine in viral encephalitis we have exploited an experimental model of Japanese encephalitis (JE). We report for the first time that in Japanese encephalitis, there is a progressive decline in level of IL-10. The extent of progressive decrease in IL-10 level following viral infection is inversely proportional to the increase in the level of proinflammatory cytokines as well as negative consequences that follows viral infection. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neuroscience Letters Elsevier

Japanese encephalitis virus infection decrease endogenous IL-10 production: Correlation with microglial activation and neuronal death

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Publisher
Elsevier
Copyright
Copyright © 2007 Elsevier Ireland Ltd
ISSN
0304-3940
D.O.I.
10.1016/j.neulet.2007.04.071
Publisher site
See Article on Publisher Site

Abstract

The anti-inflammatory cytokine interleukin (IL)-10 is synthesized in the central nervous system (CNS) and acts to limit clinical symptoms of stroke, multiple sclerosis, Alzheimer's disease, meningitis, and the behavioral changes that occur during bacterial infections. Expression of IL-10 is critical during the course of most major diseases in the CNS and promotes survival of neurons and all glial cells in the brain by blocking the effects of proinflammatory cytokines and by promoting expression of cell survival signals. In order to assess functional importance of this cytokine in viral encephalitis we have exploited an experimental model of Japanese encephalitis (JE). We report for the first time that in Japanese encephalitis, there is a progressive decline in level of IL-10. The extent of progressive decrease in IL-10 level following viral infection is inversely proportional to the increase in the level of proinflammatory cytokines as well as negative consequences that follows viral infection.

Journal

Neuroscience LettersElsevier

Published: Jun 13, 2007

References

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