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J Neuroimmunol ; 239(1-2): 44-52, 2011 Oct 28.
Article in English | MEDLINE | ID: mdl-22000153

ABSTRACT

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-1ß mRNA expression increases following acute SDR; however, IL-6 mRNA expression, but not IL-1ß, is upregulated in response to chronic SDR. Furthermore, this study demonstrated SDR prior to infection increases infection related central IL-6 and IL-1ß mRNA expression, and administration of IL-6 neutralizing antibody during SDR reverses this increase in neuroinflammation.


Subject(s)
Encephalitis, Viral/immunology , Encephalitis, Viral/pathology , Gene Expression Regulation, Viral/immunology , Interleukin-6/metabolism , Social Environment , Stress, Psychological/immunology , Stress, Psychological/pathology , Theilovirus/immunology , Animals , Chronic Disease , Disease Models, Animal , Encephalitis, Viral/genetics , Interleukin-1beta/biosynthesis , Interleukin-1beta/genetics , Interleukin-6/biosynthesis , Interleukin-6/genetics , Male , Mice , Mice, Inbred BALB C , Multiple Sclerosis/immunology , Multiple Sclerosis/pathology , Multiple Sclerosis/virology , Random Allocation , Stress, Psychological/genetics , Up-Regulation/genetics , Up-Regulation/immunology
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