Effects of Sleep on the Production of Cytokines in Humans
Abstract
The restorative functions of sleep may affect immunologic functioning. The present study examined the effects of sleep on stimulated cytokine release in 13 healthy men. The subjects spent 2 experimental nights in the sleep laboratory. In one condition, lights were turned off at 11:00 PM to enable sleep for 3.5 hours. Thereafter, they stayed awake till 7:00 AM. In the other condition, conversely, subjects stayed awake between 11:00 PM and 3:00 AM. Then, lights were turned off for a 3.5-hour phase of sleep. Blood was sampled every 30 minutes between 11:00 PM and 7:00 AM. Sleep was monitored by polysomnographic recordings. Release of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) was determined after stimulation of mononuclear cells with lipopolysaccharide from Escherichia coli. The release of IL-2 was stimulated with phytohemagglutinin. Compared with wakefulness, after 3 hours of sleep, production of TNF-alpha and IL-1 beta was substantially diminished (p < .01). Production of IL-2 was enhanced during sleep (p < .05), with this effect being limited to the second nocturnal sleep phase after 3:00 AM. Sleep-dependent changes in stimulated cytokine release were independent of changes in plasma cortisol concentrations. These results indicate a specific reducing effect of sleep (vs. wakefulness) on cytokine production by monocytes (TNF-alpha and IL-1 beta). The rather slow development of the effects calls for further studies to establish the exact time course of the influence of sleep on cytokine production.
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PGD2, the most abundant prostanoid in the brain of rodents, is a potent sleep-promoting substance in rats and mice.
“PGD2, the most abundant prostanoid in the brain of rodents, as a potent, sleep-promoting substance in rats and mice (reviewed in Refs. 246, 551).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [551]
Collectively, there is ample evidence that IL-1 and TNF, in particular, and PGD2 play a critical role in the regulation of physiological, spontaneous NREM sleep in animals, and potentially in humans, while they may not be involved in physiological REM sleep regulation.
“Collectively, there is ample evidence that IL-1 and TNF, in particular, and PGD2, play a critical role in the regulation of physiological, spontaneous NREM sleep in animals, and potentially in humans, while they may not be involved in physiological REM sleep regulation (250, 551).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [551]
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- Authors
- Uthgenannt, D., Schoolmann, D., Pietrowsky, R., Fehm, H.-L., & Born, J.
- Affiliations
- University of Lübeck (DE)
- Venue
- Psychosomatic Medicine
- Published
- 1995
- Volume
- 57
- Issue
- 2
- Pages
- 97-104
- ISSN
- 0033-3174 (ISSN-L)
- OpenAlex
- W2322010248
- Cited by
- 112
- References
- 23
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 3 · 2020: 1 · 2019: 4 · 2018: 4 · 2017: 3 · 2016: 2 · 2015: 2 · 2014: 5 · 2013: 3 · 2012: 5
- FWCI
- 4.06
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Psychosomatic Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Keywords
- sleep, cytokine production, TNF-α, IL-1β, interleukin-2, monocytes, lipopolysaccharide stimulation, phytohemagglutinin stimulation, cortisol, wakefulness, immune function
- MeSH terms
- Adult, Circadian Rhythm, Humans, Hydrocortisone, Interleukin-1, Interleukin-2, Male, Sleep, Sleep Deprivation, Sleep Stages, Tumor Necrosis Factor-alpha, Cytokines
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