Immunomodulatory cytokines determine the outcome of Japanese encephalitis virus infection in mice

Biswas, S. M. ; Kar, S. ; Singh, R. ; Chakraborty, D. ; Vipat, V. ; Raut, C. G. ; Mishra, A. C. ; Gore, M. M. ; Ghosh, D. (2010) Immunomodulatory cytokines determine the outcome of Japanese encephalitis virus infection in mice Journal of Medical Virology, 82 (2). pp. 304-310. ISSN 0146-6615

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Official URL: http://onlinelibrary.wiley.com/doi/10.1002/jmv.216...

Related URL: http://dx.doi.org/10.1002/jmv.21688

Abstract

Japanese encephalitis virus (JEV) induces an acute infection of the central nervous system, the pathogenic mechanism of which is not fully understood. To investigate host response to JEV infection, 14-day-old mice were infected via the extraneural route, which resulted in encephalitis and death. Mice that received JEV immune splenocyte transfer were protected from extraneural JEV infection. Pathology and gene expression profiles were then compared in brains of mice that either succumbed to JEV infection or were protected from infection by JEV immune cell transfer. Mice undergoing progressive JEV infection had increased expression of proinflammatory cytokines, chemokines, and signal transducers associated with the interferon (IFN) pathway. In contrast, mice receiving immune cell transfer had increased production of the Th2 cytokine IL-4, and of IL-10, with subdued expression of IFN-γ. We observed IL-10 to be an important factor in determining clinical outcome in JEV infection. Data obtained by microarray analysis were further confirmed by quantitative RT-PCR. Together, these data suggest that JEV infection causes an unregulated inflammatory response that can be countered by the expression of immunomodulatory cytokines in mice that survive lethal infection.

Item Type:Article
Source:Copyright of this article belongs to John Wiley and Sons.
Keywords:Japanese Encephalitis; Microarray; Adoptive Transfer; Splenocytes
ID Code:73607
Deposited On:06 Dec 2011 11:04
Last Modified:06 Dec 2011 11:04

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