Cited by 62Circadian rhythm and melatoninSleep and Wakefulness ResearchSleep and Work-Related Fatigue

Diurnal and sleep–wake dependent variations of soluble TNF- and IL-2 receptors in healthy volunteers

Haack, Monika, Pollmächer, Thomas, Mullington, Janet M.·2004·Brain, Behavior, and Immunity

Abstract

There is very little published information on the diurnal variation of cytokines and their receptors, in healthy individuals during normal sleep-wake patterns or during sustained wakefulness. The aim of the current investigation was to characterize concentrations of soluble tumor necrosis factor receptors (sTNF-Rs) and interleukin-2 receptor (sIL-2R) during normal sleep and wakefulness, as well as during a 24 h vigil. Plasma levels of the sTNF-R p55, sTNF-R p75, and sIL-2R did not differ significantly between nocturnal sleep and nocturnal wakefulness. Rhythmic analysis (2-h intervals) revealed significant diurnal variations for both sTNF-R p55 and sTNF-R p75, but not levels of sIL-2R. Diurnal variations of both sTNF-Rs were characterized by a single cosine curve with an average peak near 06:00 h in the morning. This peak occurred well before that of cortisol, and fluctuated inversely with the diurnal rhythm of temperature. These diurnal variations in sTNF-Rs levels are consistent with the hypothesis that the TNF system plays a role in normal diurnal temperature regulation.

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Crossref · 10.1016/j.bbi.2003.12.009

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  • Prolonged experimental sleep restriction of 10 days produced a nonsignificant increase of PGD2 and PGE2 metabolites of about 20% in healthy participants.

    “With the use of a model of prolonged experimental sleep restriction of 10 days, a nonsignificant increase of PGD2 and PGE2 metabolites of ~20% has been reported in healthy participants (223)”

    From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [223]

  • When sleep is diminished for longer than one night, plasma levels of IL-6 or CRP mostly increase, likely reflecting a systemic, unspecific inflammatory response to prolonged sleep loss.

    “More consistent findings are observed if sleep is diminished for longer than one night: plasma levels of IL-6 or CRP (which is produced by the liver in response to IL-6 secretion) mostly increase in such conditions, likely reflecting a systemic, unspecific inflammatory response to prolonged sleep loss (223, 506, 556, 564) (see also sect. IV).”

    From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [223]

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Authors
Haack, M., Pollmächer, T., & Mullington, J. M.
Affiliations
  • Beth Israel Deaconess Medical Center (US)
  • Max Planck Society (DE)
Corresponding author
Mullington, Janet M.
Venue
Brain, Behavior, and Immunity
Publisher
Elsevier BV
Published
2004-07
Volume
18
Issue
4
Pages
361-367
ISSN
0889-1591 (ISSN-L)
OpenAlex
W2078203950
Cited by
62
References
35
Citations by year
2025: 3 · 2024: 2 · 2023: 1 · 2022: 2 · 2021: 4 · 2020: 8 · 2019: 3 · 2018: 2 · 2017: 4 · 2016: 1 · 2015: 3 · 2014: 3 · 2013: 3 · 2012: 3
FWCI
0.93
Type
journal article
Language
en
Open access
closed
Locations
  • Brain Behavior and Immunity (publishedVersion)
  • PubMed (publishedVersion)
  • Max Planck Institute for Plasma Physics (submittedVersion)
Funders
National Institute of Mental Health (R01MH060641, MH 60641)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
Keywords
soluble tumor necrosis factor receptor, soluble interleukin-2 receptor, diurnal variation, sleep-wake cycle, sustained wakefulness, cytokine receptors, plasma cytokines, cortisol, healthy volunteers
MeSH terms
Adult, Analysis of Variance, Circadian Rhythm, Humans, Hydrocortisone, Male, Reference Values, Sleep, Sleep Deprivation, Wakefulness, Receptors, Interleukin-2, Antigens, CD, Receptors, Tumor Necrosis Factor, Receptors, Tumor Necrosis Factor, Type I, Receptors, Tumor Necrosis Factor, Type II

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