Sleep Deprivation and Activation of Morning Levels of Cellular and Genomic Markers of Inflammation

Irwin, Michael R.

doi:10.1001/archinte.166.16.1756

Cited by 850Sleep and Work-Related FatigueSleep and Wakefulness ResearchCircadian rhythm and melatonin

Sleep Deprivation and Activation of Morning Levels of Cellular and Genomic Markers of Inflammation

Irwin, Michael R.·2006·Archives of Internal Medicine

DOI 10.1001/archinte.166.16.1756

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Abstract

BACKGROUND: Inflammation is associated with increased risk of cardiovascular disorders, arthritis, diabetes mellitus, and mortality. The effects of sleep loss on the cellular and genomic mechanisms that contribute to inflammatory cytokine activity are not known. METHODS: In 30 healthy adults, monocyte intracellular proinflammatory cytokine production was repeatedly assessed during the day across 3 baseline periods and after partial sleep deprivation (awake from 11 pm to 3 am). We analyzed the impact of sleep loss on transcription of proinflammatory cytokine genes and used DNA microarray analyses to characterize candidate transcription-control pathways that might mediate the effects of sleep loss on leukocyte gene expression. RESULTS: In the morning after a night of sleep loss, monocyte production of interleukin 6 and tumor necrosis factor alpha was significantly greater compared with morning levels following uninterrupted sleep. In addition, sleep loss induced a more than 3-fold increase in transcription of interleukin 6 messenger RNA and a 2-fold increase in tumor necrosis factor alpha messenger RNA. Bioinformatics analyses suggested that the inflammatory response was mediated by the nuclear factor kappaB inflammatory signaling system as well as through classic hormone and growth factor response pathways. CONCLUSIONS: Sleep loss induces a functional alteration of the monocyte proinflammatory cytokine response. A modest amount of sleep loss also alters molecular processes that drive cellular immune activation and induce inflammatory cytokines; mapping the dynamics of sleep loss on molecular signaling pathways has implications for understanding the role of sleep in altering immune cell physiologic characteristics. Interventions that target sleep might constitute new strategies to constrain inflammation with effects on inflammatory disease risk.

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From Interacting epidemics? Sleep curtailment, insulin resistance, and obesity (2012) · cites this paper as [107]
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From Interacting epidemics? Sleep curtailment, insulin resistance, and obesity (2012) · cites this paper as [107]

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Authors: Irwin, M. R.
Affiliations: University of California, Los Angeles (US)
Corresponding author: Irwin, Michael R.
ORCID: Irwin, Michael R.
Venue: Archives of Internal Medicine
Publisher: American Medical Association (AMA)
Published: 2006-09-18
Volume: 166
Issue: 16
Pages: 1756
ISSN: 0003-9926 (ISSN-L)
DOI: 10.1001/archinte.166.16.1756
OpenAlex: W2148230248
Cited by: 850
References: 44
Citations by year: 2026: 30 · 2025: 54 · 2024: 48 · 2023: 45 · 2022: 65 · 2021: 42 · 2020: 41 · 2019: 42 · 2018: 44 · 2017: 41 · 2016: 48 · 2015: 54 · 2014: 36 · 2013: 59 · 2012: 48
FWCI: 36.16
Type: journal article
Language: en
Open access: closed
Locations: Archives of Internal Medicine (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute on Alcohol Abuse and Alcoholism (AA13239, R01AA013239)
National Institute on Aging (AG 18367, R01AG018367)
National Heart, Lung, and Blood Institute (HL 079955, R01HL079955)
National Institute of Mental Health (MH-55253, R01MH055253, T32MH019925, T32 MH 19925)
National Institute on Drug Abuse (R01DA016541, DA 16541)
National Institute of Allergy and Infectious Diseases (AI 52737, R01AI052737)
National Center for Research Resources (M-01RR00827, (M01 RR00865), M01RR000865, M01RR000827)
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: sleep deprivation, inflammation, monocytes, interleukin-6, TNF-α, inflammatory cytokines, cytokine gene transcription, NF-κB signaling, leukocyte gene expression, immune activation
MeSH terms: Adult, Female, Flow Cytometry, Humans, Male, Middle Aged, Monocytes, RNA, Messenger, Sleep Deprivation, Transcription, Genetic, Tumor Necrosis Factor-alpha, Biomarkers, Interleukin-6, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling

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Sleep Deprivation and Activation of Morning Levels of Cellular and Genomic Markers of Inflammation

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