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NLRP3 inflammasome: key mediator of neuroinflammation in murine Japanese encephalitis.


ABSTRACT:

Background

Japanese Encephalitis virus (JEV) is a common cause of acute and epidemic viral encephalitis. JEV infection is associated with microglial activation resulting in the production of pro-inflammatory cytokines including Interleukin-1 ? (IL-1?) and Interleukin-18 (IL-18). The Pattern Recognition Receptors (PRRs) and the underlying mechanism by which microglia identify the viral particle leading to the production of these cytokines is unknown.

Methodology/principal findings

For our studies, we have used murine model of JEV infection as well as BV-2 mouse microglia cell line. In this study, we have identified a signalling pathway which leads to the activation of caspase-1 as the key enzyme responsible for the maturation of both IL-1? and IL-18 in NACHT, LRR and PYD domains-containing protein-3 (NLRP3) dependent manner. Depletion of NLRP3 results in the reduction of caspase-1 activity and subsequent production of these cytokines.

Conclusion/significance

Our results identify a mechanism mediated by Reactive Oxygen Species (ROS) production and potassium efflux as the two danger signals that link JEV infection to caspase-1 activation resulting in subsequent IL-1? and IL-18 maturation.

SUBMITTER: Kaushik DK 

PROVIDER: S-EPMC3290554 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature

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Publications

NLRP3 inflammasome: key mediator of neuroinflammation in murine Japanese encephalitis.

Kaushik Deepak Kumar DK   Gupta Malvika M   Kumawat Kanhaiya Lal KL   Basu Anirban A  

PloS one 20120229 2


<h4>Background</h4>Japanese Encephalitis virus (JEV) is a common cause of acute and epidemic viral encephalitis. JEV infection is associated with microglial activation resulting in the production of pro-inflammatory cytokines including Interleukin-1 β (IL-1β) and Interleukin-18 (IL-18). The Pattern Recognition Receptors (PRRs) and the underlying mechanism by which microglia identify the viral particle leading to the production of these cytokines is unknown.<h4>Methodology/principal findings</h4>  ...[more]

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