Restraint stress fails to render C57BL/6 mice susceptible to Theiler's virus-induced demyelination

• Published in: Neuroimmunomodulation Vol. 17; no. 2; p. 109
• Main Authors: Steelman, Andrew J, Alford, Eric, Young, Colin R, Welsh, Thomas H, Meagher, Mary W, Welsh, C Jane R
• Format: Journal Article
• Language: English
• Published: Switzerland 01.01.2010
• Subjects: Adaptive Immunity - immunology; Animals; Cardiovirus Infections - immunology; Cardiovirus Infections - psychology; Central Nervous System - immunology; Central Nervous System - pathology; Central Nervous System - virology; Demyelinating Autoimmune Diseases, CNS - immunology; Demyelinating Autoimmune Diseases, CNS - physiopathology; Demyelinating Autoimmune Diseases, CNS - psychology; Disease Models, Animal; Disease Susceptibility - immunology; Disease Susceptibility - psychology; Female; Genetic Predisposition to Disease - genetics; Immune Tolerance - genetics; Immune Tolerance - immunology; Mice; Mice, Inbred C57BL; Movement Disorders - immunology; Movement Disorders - physiopathology; Nerve Fibers, Myelinated - immunology; Nerve Fibers, Myelinated - pathology; Nerve Fibers, Myelinated - virology; Neurons - immunology; Neurons - pathology; Neurons - virology; Restraint, Physical - adverse effects; Restraint, Physical - psychology; Stress, Psychological - immunology; Theilovirus - immunology; Viral Load - immunology
• ISSN: 1423-0216
• DOI: 10.1159/000258694

Multiple sclerosis is a degenerative disease of the CNS with a pathology consistent with immunological mediation. Although its cause is unknown, multiple factors are thought to influence both the onset and exacerbation of the disease, including both genetic background as well as environmental factors. We are interested in the effect of psychological stress on the onset and exacerbation of Theiler's virus-induced demyelinating disease (TVID), a murine model of MS in which viral persistence facilitates demyelination. In the current study, we determined whether chronic restraint stress (RS)-induced immunosuppression could result in the establishment of a persistent CNS infection in the normally TVID-resistant C57BL/6 mouse strain, resulting in demyelination. Our data indicated that RS repeated over the course of 7 days was not sufficient to cause decreases in virus-specific adaptive immunity, and did not significantly alter CNS viral levels. Furthermore, chronic repeated RS lasting until 4 weeks after infection altered neither the development of virus-specific IgG nor motor function determined by Rotarod analysis. In addition, histological analysis of the CNS of stressed mice indicated no inflammation or demyelination on day 193 after infection. These results suggest that stress alone is not sufficient to overcome genetic resistance to TVID in the C57BL/6 mouse strain.