| dc.description.abstract | Neurodegenerative diseases, such as multiple sclerosis (MS), are
adversely affected by both stress and inflammation. Theiler's murine
encephalomyelitis virus infection is an excellent animal model of MS, allowing
examination of central nervous system inflammation during the acute phase of
infection. Social disruption stress exacerbates acute Theiler's virus infection.
Both social disruption stress and Theiler's virus infection elevate the proinflammatory
cytokine, Interleukin-6 (IL-6). The current study examined the
necessity and sufficiency of IL-6 in mediating the negative effects of social
disruption stress in acute Theiler's virus infection. Experiment 1 blocked IL-6
function with a neutralizing antibody administered simultaneously with social
disruption stress. All mice were then infected, and measures of illness, motor
impairment and physiological signs of disease were collected up to 21 d postinfection.
Experiment 2 administered exogenous IL-6 for one week (replacing
social disruption with the cytokine treatment), followed by infection. Measures identical to those collected in Experiment 1 were collected for up to 21 d postinfection.
Results indicate that IL-6 is necessary for the development of the
sickness, motor impairment, and immunological effects of social stress in acute
Theiler's virus infection. In contrast, IL-6 alone can induce some, but not all, of
the sickness behavior exacerbations, and was not sufficient for the development
of either motor impairment or immunological effects previously associated with
social disruption stress. These results have many important implications for
further research in the effects of social stress on Theiler's virus infection, as well
as clinical implications for both MS and other inflammatory mediated diseases,
such as Alzheimer's disease and Parkinson's disease. | en |
