[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 35.173.234.140. Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Original Investigation
September 18, 2006

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

Author Affiliations

Author Affiliations: Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience, and Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles.

Arch Intern Med. 2006;166(16):1756-1762. doi:10.1001/archinte.166.16.1756
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 α 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 α messenger RNA. Bioinformatics analyses suggested that the inflammatory response was mediated by the nuclear factor κB 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.

×