| Literature DB >> 24027260 |
Toru Nakamura1, Stephan Schwander, Robert Donnelly, Dane B Cook, Felix Ortega, Fumiharu Togo, Yoshiharu Yamamoto, Neil S Cherniack, Marc Klapholz, David Rapoport, Benjamin H Natelson.
Abstract
A major hypothesis regarding the cause of chronic fatigue syndrome (CFS) is immune dysregulation, thought to be reflected in upregulated proinflammatory cytokines leading to the symptoms that are characteristic of this illness. Because the symptoms worsen with physical exertion or sleep loss, we hypothesized that we could use these stressors to magnify the underlying potential pathogenic abnormalities in the cytokine systems of people with CFS. We conducted repeat blood sampling for cytokine levels from healthy subjects and CFS patients during both postexercise and total sleep deprivation nights and assayed for protein levels in the blood samples, mRNA activity in peripheral blood lymphocytes (PBLs), and function in resting and stimulated PBLs. We found that these environmental manipulations did not produce clinically significant upregulation of proinflammatory cytokines. These data do not support an important role of immune dysregulation in the genesis of stress-induced worsening of CFS.Entities:
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Year: 2013 PMID: 24027260 PMCID: PMC3837776 DOI: 10.1128/CVI.00527-13
Source DB: PubMed Journal: Clin Vaccine Immunol ISSN: 1556-679X