Cited by 119Sleep and Wakefulness ResearchSleep and Work-Related FatigueSleep and related disorders

Influence of endotoxin on nocturnal sleep in humans

Pollmacher, T., Schreiber, W., Gudewill, S., Vedder, H., Fassbender, K., Wiedemann, K., Trachsel, L., Galanos, C. +1 more·1993·American Journal of Physiology-Regulatory, Integrative and Comparative Physiology

Abstract

Sleepiness is a common complaint during infectious diseases, but the interaction between sleep and host defense mechanisms has been poorly explored in humans. We therefore studied the effect of endotoxin, a major pathophysiological factor in gram-negative bacterial infections, on sleep and on parameters of the primary host response in men. In a single-blind counterbalanced trial, 15 healthy volunteers received either placebo or Salmonella abortus equi endotoxin (0.4 ng/kg body wt) intravenously on two separate occasions. Nocturnal sleep was recorded, and rectal temperature and the plasma levels of tumor necrosis factor-alpha, interleukin-6, adrenocorticotropic hormone, and cortisol were monitored for 12 h. Endotoxin reduced the relative amounts of wakefulness (P < 0.05) and rapid-eye-movement (REM) sleep (P < 0.05) and increased the relative amount of non-REM sleep (P < 0.01). Electroencephalogram delta power during non-REM sleep, as measured by spectral analysis, was not altered by endotoxin. The endotoxin-induced changes in sleep structure were related temporally and quantitatively to the increases in rectal temperature and to the release of cytokines and neurohormones. It is concluded that cytokines and neurohormones mediate the effects of endotoxin upon sleep. The ensuing increase in non-REM sleep may be part of the adaptive host response to bacterial infections in humans.

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Crossref · 10.1152/ajpregu.1993.264.6.r1077

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  • In humans, NREM sleep enhancing or intensifying effects are restricted to times of very mild host response activation, whereas stronger responses characterized by large cytokine increases and fever caused sleep disruption.

    “in humans, NREM sleep enhancing or intensifying effects are restricted to times of very mild host response activation, whereas stronger responses characterized by large cytokine increases and fever caused sleep disruption (224, 396, 442).”

    From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [442]

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Authors
Pollmacher, T., Schreiber, W., Gudewill, S., Vedder, H., Fassbender, K., Wiedemann, K., Trachsel, L., Galanos, C., & Holsboer, F.
Affiliations
  • Max Planck Institute of Psychiatry, Department of Psychiatry, Munich, Federal Republic of Germany.
  • Max Planck Institute of Psychiatry (DE)
Venue
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Published
1993-06-01
Volume
264
Issue
6
Pages
R1077-R1083
ISSN
  • 0363-6119 (ISSN-L)
  • 1522-1490
OpenAlex
W1899504327
Cited by
119
References
0
Citations by year
2025: 4 · 2024: 5 · 2022: 2 · 2021: 4 · 2020: 5 · 2019: 2 · 2018: 5 · 2017: 4 · 2016: 2 · 2015: 10 · 2014: 2 · 2013: 4 · 2012: 2
FWCI
3.45
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
  • PubMed (publishedVersion)
  • Max Planck Institute for Plasma Physics (submittedVersion)
  • MPG.PuRe (Max Planck Society) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
Keywords
endotoxin, Salmonella abortus equi, nocturnal sleep, sleep architecture, REM sleep, NREM sleep, wakefulness, cytokines, TNF-α, interleukin-6, ACTH, cortisol, body temperature, host defense, gram-negative bacterial infection, sleepiness
MeSH terms
Adrenocorticotropic Hormone, Adult, Body Temperature, Endotoxins, Humans, Hydrocortisone, Male, Rectum, Salmonella, Sleep, Sleep Stages, Tumor Necrosis Factor-alpha, Interleukin-6

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