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

The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.

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

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

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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Crossref · 10.1001/archinte.166.16.1756

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Metadata

Authors
Irwin, M. R.
Affiliations
University of California, Los Angeles (US)
Corresponding author
Irwin, Michael R.
Venue
Archives of Internal Medicine
Published
2006-09-18
Volume
166
Issue
16
Pages
1756
ISSN
0003-9926 (ISSN-L)
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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