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REM Sleep Deprivation in Rats Results in Inflammation and Interleukin-17 Elevation
Abstract
Sleep deprivation is a major health problem in modern society. Deprivation of rapid eye movement (REM) sleep is particularly damaging to cognition and to spatial memory; however, the mechanisms that mediate these deteriorations in function are not known. We explored the possibility that REM sleep deprivation may provoke major changes in the immune system by inducing inflammation. Rats were subjected to 72 h of REM sleep deprivation, and the plasma levels of proinflammatory cytokines (IL-1, IL-1beta, IL-6, IL-17A, and TNF-alpha), an anti-inflammatory cytokine (IL-10), the inflammatory markers homocysteine, corticosterone, and hyperthermia were measured immediately after the deprivation period, and 7 days later. The results indicate that REM sleep deprivation induced an inflammatory response. The levels of the proinflammatory cytokines and markers were significantly elevated in sleep-deprived rats as compared to control rats. After 7 days of recovery, the levels of some markers, including hyperthermia, remained higher in sleep-deprived rats versus the control animals. IL-17A appears to play a pivotal role in coordinating the inflammation. These data shed new light on the mechanism of sleep deprivation-induced inflammation.
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“As shown in animals, this system allows the drainage of deep brain structures resulting from an increase of cortical interstitial space, which expands by more than 60% during sleep”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [593]
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Role of sleep deprivation in immune-related disease risk and outcomes
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The Bidirectional Relationship between Sleep and Immunity against Infections
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Regulation of the Blood–Brain Barrier by Circadian Rhythms and Sleep
Cuddapah, V. A., Zhang, S., & Sehgal, A. (2019) · Trends in Neurosciences · doi:10.1016/j.tins.2019.05.001 · Cited by 208
“Sleep restriction leads to increased activity of several pro-inflammatory mediators, including C-reactive protein [60], interleukin-1β [61] (IL-1β), interleukin-6 [62] (IL-6), interleukin-17 [63] (IL-17), interferon-γ [64] (IFNγ), and TNFα [62, 64–67].”
Background
Metadata
- Authors
- Yehuda, S., Sredni, B., Carasso, R. L., & Kenigsbuch-Sredni, D.
- Affiliations
- Bar-Ilan University (IL)
- Hillel Yaffe Medical Center (IL)
- Interdisciplinary Department, The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan, Israel.
- ORCID
- Sredni, Benjamin
- Venue
- Journal of Interferon & Cytokine Research
- Publisher
- SAGE Publications
- Published
- 2009-07
- Volume
- 29
- Issue
- 7
- Pages
- 393-398
- ISSN
- 1079-9907 (ISSN-L)
- 1557-7465
- OpenAlex
- W2024940102
- Semantic Scholar
- 0c21c44497e54bddb2003dcb6e50f30e93f94345
- Cited by
- 158
- References
- 47
- Citations by year
- 2026: 7 · 2025: 5 · 2024: 11 · 2023: 12 · 2022: 22 · 2021: 8 · 2020: 10 · 2019: 12 · 2018: 6 · 2017: 13 · 2016: 8 · 2015: 7 · 2014: 6 · 2013: 12 · 2012: 6
- FWCI
- 3.06
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Interferon & Cytokine Research (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 › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- REM sleep deprivation, sleep deprivation, inflammation, IL-17A, inflammatory cytokines, IL-1β, interleukin-6, TNF-α, IL-10, homocysteine, corticosterone, hyperthermia, immune system, sleep and immunity
- MeSH terms
- Animals, Corticosterone, Fever, Homocysteine, Inflammation, Male, Sleep Deprivation, Biomarkers, Up-Regulation, Rats, Long-Evans, Interleukin-17, Rats
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