Cited by 330Sleep and Work-Related FatigueSleep and Wakefulness ResearchCircadian rhythm and melatonin

The effects of 40 hours of total sleep deprivation on inflammatory markers in healthy young adults

Frey, Danielle J., Fleshner, Monika, Wright, Kenneth P.·2007·Brain, Behavior, and Immunity

Abstract

Inflammatory cytokines are released in response to stress, tissue damage, and infection. Acutely, this response is adaptive; however, chronic elevation of inflammatory proteins can contribute to health problems including cardiovascular, endocrine, mood, and sleep disorders. Few studies have examined how sleep deprivation acutely affects inflammatory markers, which was the aim of the current study. Nineteen healthy men and women aged 28.05+/-8.56 (mean+/-SD) were totally sleep deprived for 40 h under constant routine conditions. Pro-inflammatory markers: intracellular adhesion molecule-1 (ICAM-1), E-selectin, vascular adhesion molecule-1 (VCAM-1), c-reactive protein (CRP), interleukin-6 (IL-6), and interleukin-1beta (IL-1beta), and the anti-inflammatory cytokine interleukin-1 receptor antagonist (IL-1ra) were assayed in plasma. Daytime levels during baseline (hours 1-15 of scheduled wakefulness) were compared to daytime levels during sleep deprivation (hours 25-39 of scheduled wakefulness), thus controlling for circadian phase within an individual. Repeated measures ANOVA with planned comparisons showed that 40 h of total sleep deprivation induced a significant increase in E-selectin, ICAM-1, IL-1beta, and IL-1ra, a significant decrease in CRP and IL-6, and no significant change in VCAM-1. Alterations in circulating levels of pro- and anti-inflammatory cytokines and cell adhesion molecules during sleep deprivation were consistent with both increased and decreased inflammation. These findings suggest that one night of sleep loss triggers a stress response that includes stimulation of both pro- and anti-inflammatory proteins in the healthy young subjects tested under our experimental conditions.

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Crossref · 10.1016/j.bbi.2007.04.003

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  • One night without sleep activates vascular endothelial markers such as E-selectin and s-ICAM-1.

    “a single night of sleep loss induces an activation of vascular endothelial markers (ie, E-selectin, s-intercellular adhesion molecule, s-ICAM-1) (Frey et al, 2007;Sauvet et al, 2010).”

    From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Frey et al, 2007

  • On the basis of objectively assessed sleep, lower sleep efficiency was shown to predict higher IL-6 levels in 74 older women.

    “On the basis of objectively assessed sleep, lower sleep efficiency was shown to predict higher IL-6 levels in 74 older women”

    From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [201]

  • Laboratory studies have shown that physiologic sleep restriction is associated with a proinflammatory state, including elevations in inflammatory cytokines such as IL-1B, IL-6, IL-17, TNF-α, and C-reactive protein.

    “Laboratory studies have shown that physiologic sleep restriction is associated with a proinflamma-tory state, including elevations in inflammatory cytokines, such as interleukin 1B (IL-1B),64,65 IL-6,64,66–68 IL-17,64,69 tumor necrosis factor-α,64,68,70–72 and C-reactive protein.64,69,73–76”

    From Sleep, Health, and Society (2017) · cites this paper as [65]

  • The relationship between sleep and metabolism has been extensively studied in human subjects under varying conditions, such as total sleep deprivation, partial sleep deprivation, and sleep fragmentation.

    “The relationship between sleep and metabolism has been extensively studied in human subjects under varying conditions, such as total sleep deprivation,87–100 partial sleep deprivation,101–122 and sleep fragmentation123–125 (Table 1).”
  • Mean 24-hour plasma cortisol often remains unchanged by sleep deprivation, but circadian cortisol pattern changes.

    “Mean 24-h levels of plasma cortisol often remain unchanged by sleep deprivation,43,95,96,99,106,109,123 but the circadian cortisol-pattern changes, as described above.”

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References 50 · Cited by 330

Authors
Frey, D. J., Fleshner, M., & Wright, K. P.
Affiliations
University of Colorado Boulder (US)
Corresponding author
Wright, Kenneth P.
Venue
Brain, Behavior, and Immunity
Publisher
Elsevier BV
Published
2007-11
Volume
21
Issue
8
Pages
1050-1057
ISSN
0889-1591 (ISSN-L)
OpenAlex
W2111173867
Cited by
330
References
50
Citations by year
2026: 16 · 2025: 22 · 2024: 19 · 2023: 11 · 2022: 18 · 2021: 14 · 2020: 23 · 2019: 12 · 2018: 13 · 2017: 16 · 2016: 24 · 2015: 29 · 2014: 19 · 2013: 19 · 2012: 23
FWCI
13.70
Type
journal article
Language
en
Open access
closed
Locations
  • Brain Behavior and Immunity (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Harold Whitworth Pierce Charitable Trust
  • National Institutes of Health
  • National Institute on Aging (F32 T32-AG15332, R01-AG00279)
  • National Heart, Lung, and Blood Institute (R01HL073196)
  • National Institute of Mental Health (R01 MH45130, R01MH045130)
  • National Center for Research Resources (M01 RR 02635, M01RR002635)
Topics
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
Keywords
total sleep deprivation, inflammatory markers, cytokines, IL-1β, interleukin-1 receptor antagonist, interleukin-6, C-reactive protein, adhesion molecules, ICAM-1, E-selectin, VCAM-1, acute stress response, circadian phase, healthy young adults
MeSH terms
Acute-Phase Reaction, Adaptation, Physiological, Adult, Analysis of Variance, C-Reactive Protein, Female, Amine Oxidase (Copper-Containing), Humans, Male, Reference Values, Sleep Deprivation, Stress, Physiological, Time Factors, Biomarkers, Cell Adhesion Molecules, Interleukin-6, Cytokines, Intercellular Adhesion Molecule-1, E-Selectin, Interleukin-1beta, Interleukin 1 Receptor Antagonist Protein

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