Social disruption induced priming of CNS inflammatory response to Theiler's virus is dependent upon stress induced IL-6 release.
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Chronic social disruption stress (SDR) exacerbates acute and chronic phase Theiler's murine encephalomyelitis virus (TMEV) infection, a mouse model of multiple sclerosis. However, the precise mechanism by which this occurs remains unknown. The present study suggests that SDR exacerbates TMEV disease course by priming virus-induced neuroinflammation. It was demonstrated that IL-1 mRNA expression increases following acute SDR; however, IL-6 mRNA expression, but not IL-1, is upregulated in response to chronic SDR. Furthermore, this study demonstrated SDR prior to infection increases infection related central IL-6 and IL-1 mRNA expression, and administration of IL-6 neutralizing antibody during SDR reverses this increase in neuroinflammation.