ArticlePhysiology & behavior2008
Glucocorticoid exposure alters the pathogenesis of Theiler's murine encephalomyelitis virus during acute infection.
Article in Physiology & behavior, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Chronic social stress impairs virus specific adaptive immunity during acute Theiler's virus infection.Journal of neuroimmunology · 2013Article
- A marked reduction in priming of cytotoxic CD8+ T cells mediated by stress-induced glucocorticoids involves multiple deficiencies in cross-presentation by dendritic cells.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Chronic restraint stress during early Theiler's virus infection exacerbates the subsequent demyelinating disease in SJL mice: II. CNS disease severity.Journal of neuroimmunology · 2010Article
- Neonatal maternal separation alters immune, endocrine, and behavioral responses to acute Theiler's virus infection in adult mice.Behavior genetics · 2010Article
- Stress-induced glucocorticoids at the earliest stages of herpes simplex virus-1 infection suppress subsequent antiviral immunity, implicating impaired dendritic cell function.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Restraint stress modulates virus specific adaptive immunity during acute Theiler's virus infection.Brain, behavior, and immunity · 2009Article
- Neuroimmune interactions in a model of multiple sclerosis.Annals of the New York Academy of Sciences · 2009Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Previous research has shown that chronic restraint stress exacerbates Theiler's virus infection, a murine model for CNS inflammation and multiple sclerosis. The current set of experiments was designed to evaluate the potential role of glucocorticoids in the deleterious effects of restraint stress on acute CNS inflammatory disease. Exposure to chronic restraint stress resulted in elevated levels of corticosterone as well as increased clinical scores and weight loss (Experiment 1). In addition, corticosterone administration alone exacerbated behavioral signs of TMEV-induced sickness (i.e. decreased body weight, increased symptoms of encephalitis, and increased mortality) and reduced inflammation in the CNS (Experiment 2). Infected subjects receiving exogenous corticosterone showed exacerbation of acute phase measures of sickness and severe mortality as well as decreased viral clearance from CNS (Experiment 3). These findings indicate that corticosterone exposure alone is sufficient to exacerbate acute CNS inflammatory disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.