Article

Sleep deprivation and activation of morning levels of cellular and genomic markers

Department of Psychiatry and Biobehavioural Sciences, University of California, Los Angeles, Los Ángeles, California, United States
Archives of Internal Medicine (Impact Factor: 17.33). 10/2006; 166(16):1756-62. DOI: 10.1001/archinte.166.16.1756
Source: PubMed

ABSTRACT

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.
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.
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.
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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    • "Sleep interferes with the immune system and the inflammatory response[4]and in a study of 30 adults who were sleep deprived (sleep limited to 3 a.m. to 7 a.m.), researchers found monocyte production of interleukin-6 and tumor necrosis factor alpha to be significantly increased[14]; however, in a study of 19 participants who underwent 40 hours of total sleep deprivation, although there was a significant increase in interleukin-1beta and interleukin-1ra, there was a significant decrease in c-reactive protein and interleukin-6[15]. There is a need to further study the influence of routine sleep patterns upon the biological markers. "
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    • "Sleep loss has been associated with increased inflammation in humans and acts as a risk factor for development of chronic disease, notably cardiovascular and metabolic chronic diseases[8,21,25]. Although the exact mechanisms linking sleep loss to these various pathologies are incompletely understood, epidemiological and empirical studies have suggested that sleep loss promotes exaggerated inflammatory responses in brain and in the periphery[13,14,30,31]. Abbreviations: IL-1, interleukin-1-beta; MMP, modified multiple platform; PSD, paradoxical sleep deprivation; REM, rapid-eye movement; TGF1, transforming growth factor-beta-1; TNF, tumor necrosis factor-alpha. "
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    • "In shorter human experiments the results were not so consistent (reviewed in Motivala 2011). However, even 1 day of partial sleep deprivation produces many short lasting disturbances in immunity, like reduction of activity of natural killers and lymphokine-activated killers or the suppression of IL-2 production (Irwin et al. 2006). The important implication from human studies is that adequate sleep period shortens the time of viral infection (Cohen et al. 2009). "
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