Sleep Loss Activates Cellular Inflammatory Signaling
Open accessAbstract
Background Accumulating evidence suggests that sleep disturbance is associated with inflammation and related disorders including cardiovascular disease, arthritis, and diabetes mellitus. This study was undertaken to test the effects of sleep loss on activation of nuclear factor (NF)-kappaB, a transcription factor that serves a critical role in the inflammatory signaling cascade.Methods In 14 healthy adults (seven women; seven men), peripheral blood mononuclear cell NF-kappaB was repeatedly assessed, along with enumeration of lymphocyte subpopulations, in the morning after baseline sleep, partial sleep deprivation (awake from 11 pm to 3:00 am), and recovery sleep.Results In the morning after a night of sleep loss, mononuclear cell NF-kappaB activation was significantly greater compared with morning levels following uninterrupted baseline or recovery sleep, in which the response was found in female but not in male subjects.Conclusions These results identify NF-kappaB activation as a molecular pathway by which sleep disturbance may influence leukocyte inflammatory gene expression and the risk of inflammation-related disease.
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Following sleep deprivation in the first night half, TNF production in monocytes and TNF mRNA are increased in the morning.
“Following sleep deprivation in the first night half, TNF production in monocytes and TNF mRNA were shown to be increased in the morning (256, 262, 264).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [264]
Spontaneous production of IL-6 and TNF by monocytes was increased in the morning after a night of sleep restriction, and this increase persisted in those monocytes that co-produced IL-6 and TNF after a night of recovery sleep.
“Spontaneous production of IL-6 and TNF by monocytes was increased in the morning after a night of sleep restriction, and this increase persisted in those monocytes that co-produced IL-6 and TNF after a night of recovery sleep (264).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [264]
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- Authors
- Irwin, M. R., Wang, M., Ribeiro, D., Cho, H. J., Olmstead, R., Breen, E. C., Martinez-Maza, O., & Cole, S.
- Affiliations
- University of California, Los Angeles (US)
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2008-09
- Volume
- 64
- Issue
- 6
- Pages
- 538-540
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC2547406
- OpenAlex
- W2082307168
- Cited by
- 467
- References
- 21
- Citations by year
- 2026: 24 · 2025: 29 · 2024: 35 · 2023: 35 · 2022: 42 · 2021: 29 · 2020: 27 · 2019: 22 · 2018: 21 · 2017: 25 · 2016: 27 · 2015: 25 · 2014: 30 · 2013: 21 · 2012: 22
- FWCI
- 24.04
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Alcohol Abuse and Alcoholism (R01AA013239)
- National Institute on Aging (AG 026364, R01AG026364, P30AG028748)
- National Heart, Lung, and Blood Institute (HL 079955, R01HL079955)
- National Institute of Mental Health (T32-MH-18399, T32MH019925, T32MH018399)
- National Cancer Institute (R01CA116778, CA-10014152, CA-116778, R01CA119159)
- National Center for Research Resources (M01RR000865, RR00827, 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, NF-κB activation, inflammatory signaling, peripheral blood mononuclear cells, lymphocyte subsets, sex differences, recovery sleep, sleep disorders
- MeSH terms
- Adult, Cardiovascular Diseases, Diabetes Mellitus, Female, Humans, Inflammation, Sleep Initiation and Maintenance Disorders, Lymphocytes, Male, Sleep Deprivation, Tumor Necrosis Factor-alpha, Signal Transduction, Antigens, CD, Interleukin-6, NF-kappa B
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