markers eg IL6 TNF prostaglandins robustly respond to acute sleep deficiency whether measured in urine plasma or immune cells It has been repeatedly shown that these markers do not return ID: 802394
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Slide1
Introduction
Various pro-inflammatory
markers
(e.g., IL-6, TNF, prostaglandins) robustly respond to acute sleep deficiency, whether measured in urine, plasma, or immune cells. It has been repeatedly shown that these markers do not return to baseline after one or two nights of recovery sleep, suggesting that acute sleep deficiency may disrupt the process of inflammatory resolution. This poster introduces markers involved in resolution physiology, which has been mainly studied in pre-clinical animal models, but may give promise to human translation.
The resolution of inflammation is an active, rather than passive process. The newly discovered lipid mediators resolvins, maresins, lipoxins, and protectins (Serhan et al., 2015) are part of this active biochemical program enabling the resolution of inflammation and the return to baseline (Figure 1). These lipid mediators derive from polyunsaturated fatty acids (PUFA), such as the omega-3 PUFAs EPA and DHA, and can stimulate key cellular events (counter-regulation of chemokines/cytokines, cessation of neutrophil tissue infiltration, stimulation of macrophage-mediated actions etc.).
Since proresolving markers have never been measured in the context of sleep, we first investigated whether they are detectable in human plasma of healthy young participants, and whether they respond to acute sleep deficiency followed by recovery sleep.
Conclusion
First results from this work-in-progress suggest that acute sleep deficiency not only affects proinflammatory markers, but also markers contributing to the active process of inflammatory resolution.The balance between proinflammatory and proresovling markers may be an area ripe for exploring as an inflammatory-related biomarker of acute and chronic sleep deficiency.
Preliminary data
References.Serhan CN, Chiang N, Dalli J, Levy BD. Lipid Mediators in the Resolution of Inflammation. Cold Spring Harbor Perspectives in Biology 2015;7.
Does acute sleep deficiency affect markers of inflammatory resolution?
Monika Haack,
Vrushank Bhatt, Moussa, Diolombi, Janet MullingtonDepartment of Neurology, Beth Israel Deaconess Medical Center, Boston, MA
How does inflammation resolve?
Figure 1
: Lipid-mediator biosynthesis in the resolution of acute inflammation that enables the return to baseline. Adapted from Serhan et al., 2015.
Methods:Measurement of inflammatory and proresolving markers in blood obtained from an experimental model resembling common sleep-wake behaviors of restricting sleep during week/work days and catching up on sleep during weekend/ work-off days. Measures: IL-6 positive monocytes after stimulation with LPS, quantified with flow cyto-metry. Proresolving markers de-termined in plasma, using liquid chromatography-tan- dem mass spectrometry (LC-MS-MS; Lipid Mediator Metabololipidomics Core, Brigham and Women’s Hospital Boston, Director Prof. Serhan).
Results:
Figure 2
: IL-6 positive monocytes increase upon repeated exposure to sleep restriction, without returning to baseline levels after intermittent recovery sleep (N=14). The pro-resolving lipid mediator resolvin E3 decreases after 5 nights of restricted sleep, and further decreases upon 2 nights of recovery sleep, suggesting that sleep deficiency interferes with the active process of inflammatory resolution (N=2).
Support.
NHLBI
R01 HL105544 to MH; National Center of Research Resources
UL1 TR001102 to the Harvard Clinical and Translational Science Center
.
mhaack@bidmc.harvard.edu