Elsevier

Biological Psychiatry

Volume 64, Issue 6, 15 September 2008, Pages 538-540
Biological Psychiatry

Brief Report
Sleep Loss Activates Cellular Inflammatory Signaling

https://doi.org/10.1016/j.biopsych.2008.05.004Get rights and content

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)-κB, 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-κB 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-κB 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-κB activation as a molecular pathway by which sleep disturbance may influence leukocyte inflammatory gene expression and the risk of inflammation-related disease.

Section snippets

Methods and Materials

Fourteen subjects (seven men and seven women) who were medically healthy, as determined by medical history, physical examination, and laboratory testing, were recruited between October 2006 and June 2007. All subjects fulfilled criteria for Never Mentally Ill as determined by Structured Clinical Interview for Diagnostic and Statistical Manual—IV (SCID) (mean age = 51.8 years [SD = 12.8]; 50% women; mean education level = 15.8 years [SD = 4.6]; mean body mass index [BMI] = 26.9 [SD = 3.6]; 35.7%

Results

Subjects displayed an increase of PBMC NF-κB activation after PSD [condition effect: F(2,82.0) = 7.0, p < .01; Figure 1A]. Pairwise comparisons showed that levels of NF-κB activation were markedly increased the morning after PSD compared with baseline- and recovery morning levels (−.054, 95% confidence interval −.099 to −.009 ng NF-κB protein/μg total nuclear protein, p < .01; .057, .019–.156, 95% confidence interval, p < .01), with a 30% increase relative to baseline levels. Levels of NF-κB

Discussion

Here we present evidence that acute sleep loss induces a rapid increase in activation of the transcription factor NF-κB in PBMC, providing a potential molecular mechanism for the effects of sleep loss on proinflammatory gene expression and circulating levels of inflammatory mediators (7, 8, 10). This observation that sleep loss results in nuclear translocation of NF-κB verifies previous bioinformatic indications (10) and closes an important gap in understanding the cellular mechanisms by which

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