Restraint stress modulates virus specific adaptive immunity during acute Theiler’s virus infection

Steelman, Andrew J.; Dean, Dana D.; Young, Colin R.; Smith, Roger; Prentice, Thomas W.; Meagher, Mary W.; Welsh, C. Jane

doi:10.1016/j.bbi.2009.03.010

Cited by 27 publications

(42 citation statements)

References 107 publications

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“…In support of this, it has been demonstrated that stress can modify T cell responses (Sommershof et al, 2010; Steelman et al, 2009). For example, Young and colleagues (submitted) demonstrate that infection related increases in virus-specific CD4+ and CD8+ T cells within the CNS are significantly attenuated due to SDR exposure.…”

Section: Discussionmentioning

confidence: 80%

Social disruption induced priming of CNS inflammatory response to Theiler's virus is dependent upon stress induced IL-6 release

Vichaya

Young

Frazier

et al. 2011

Journal of Neuroimmunology

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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 SDR exacerbates TMEV disease course by priming virus-induced neuroinflammation. It was demonstrated that IL-1β mRNA expression increases following acute SDR; however, IL-6 mRNA expression, but not IL-1β, is upregulated in response to chronic SDR. Furthermore, this study demonstrated SDR prior to infection increases infection related central IL-6 and IL-1β mRNA expression, and administration of IL-6 neutralizing antibody during SDR reverses this increase in neuroinflammation.

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Section: Discussionmentioning

confidence: 80%

Social disruption induced priming of CNS inflammatory response to Theiler's virus is dependent upon stress induced IL-6 release

Vichaya

Young

Frazier

et al. 2011

Journal of Neuroimmunology

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“…However, previous studies reported chronic stress increased the plasma level of IL-6and TNF-α 24, 25 , while another report showed that restraint stress caused a significant decrease in the concentrations of circulating IFN-γ, IL-12(p40), IL-12(p70), IL-4, and IL-5 26 . Recently, Smith et al .…”

Section: Discussionmentioning

confidence: 88%

Spleen contributes to restraint stress induced changes in blood leukocytes distribution

Jiang

Sun

et al. 2017

Sci Rep

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Psychological stress has great impacts on the immune system, particularly the leukocytes distribution. Although the impacts of acute stress on blood leukocytes distribution are well studied, however, it remains unclear how chronic stress affects leukocytes distribution in peripheral circulation. Furthermore, there is no report about the role of spleen in the blood leukocytes distribution induced by stress. Here we show that spleen contributes to the alteration of restraint stress induced blood leukocytes distribution. Our data confirmed that restraint stress induced anxiety-like behavior in mice. Furthermore, we found that restraint stress decreased the CD4/CD8 ratio and elevated the percentages of natural killer cells, monocytes and polymorphonuclear myeloid-derived suppressor cell. We demonstrated that activation of hypothalamic-pituitary-adrenal axis (HPA) and sympathetic nervous system (SNS) contributes to restraint stress induced alteration of blood leukocyte distribution. Interestingly, we found that splenectomy could reverse the change of CD4/CD8 ratio induced by restraint stress. Together, our findings suggest that activation of HPA axis and SNS was responsible for the blood leukocyte subsets changes induced by restraint stress. Spleen, at least in part, contributed to the alteration in peripheral circulation induced by restraint stress.

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“…During early infection with TMEV, RS CBA mice develop decreased NK-cell activity [33] and chemokine/cytokine expression in the brains and spleens, as well as altered viral dissemination and viral load [31,35,49] . Additionally, in SJL mice, RS suppresses virus-specific T-cell responses in the CNS as well as the periphery [50] , which may result in an exacerbated late disease [29] .…”

Section: Discussionmentioning

confidence: 99%

Restraint Stress Fails to Render C57BL/6 Mice Susceptible to Theiler’s Virus-Induced Demyelination

Steelman¹,

Alford²,

Young³

et al. 2009

Neuroimmunomodulation

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Objectives: 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. Methods: 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. Results: 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. Conclusion: These results suggest that stress alone is not sufficient to overcome genetic resistance to TVID in the C57BL/6 mouse strain.

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Restraint stress modulates virus specific adaptive immunity during acute Theiler’s virus infection

Cited by 27 publications

References 107 publications

Social disruption induced priming of CNS inflammatory response to Theiler's virus is dependent upon stress induced IL-6 release

Social disruption induced priming of CNS inflammatory response to Theiler's virus is dependent upon stress induced IL-6 release

Spleen contributes to restraint stress induced changes in blood leukocytes distribution

Restraint Stress Fails to Render C57BL/6 Mice Susceptible to Theiler’s Virus-Induced Demyelination

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