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Neuroimmune Interactions in a Model of Multiple Sclerosis
Author(s) -
Welsh C. Jane,
Steelman Andrew J.,
Mi Wentao,
Young Colin R.,
Storts Ralph,
Welsh, Jr Thomas H.,
Meagher Mary W.
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2008.03984.x
Subject(s) - multiple sclerosis , immunology , immune system , neuroinflammation , immunosuppression , experimental autoimmune encephalomyelitis , virus , demyelinating disease , neuroimmunology , exacerbation , disease , chemokine , encephalomyelitis , central nervous system , innate immune system , biology , medicine , inflammation , neuroscience
Psychological stress has been implicated in both the onset and exacerbation of multiple sclerosis (MS). Our research has focused on the role of stress at the onset of MS, using the mouse model Theiler's murine encephalomyelitis virus‐induced demyelination. Theiler's virus is a natural pathogen of mice that causes a persistent infection of the central nervous system (CNS) and inflammatory immune‐mediated demyelination that is very similar to MS. Our research has shown that restraint stress sufficiently increases corticosterone secretion to cause immunosuppression. Stressed mice develop decreased innate and adaptive immune responses, including decreased chemokine and cytokine responses, to virus, which leads to increased viral replication within the CNS. Higher levels of virus then cause increased later demyelinating disease. These findings may have important implications in our understanding of the interactions between stress and the development of autoimmune diseases induced by infectious agents.