Sleep profoundly influences immune and inflammatory responses, protecting against age-associated immune disorders including cardiovascular disease, cancer, and neurodegenerative diseases.
“What we are learning is that sleep modulates the production of cells that are the main actors of inflammation” said Filip K. Swirski, Ph.D., a senior study author and director of the Cardiovascular Research Institute at Icahn School of Medicine at Mount Sinai, New York City.
Most adults should get 7-8 hours of uninterrupted sleep each night. Older adults need about 7-9 hours, while children ages 11-17 need about 8-10 hours.
Adults who cut back on sleep for six weeks had increased markers of inflammation.
Good, quality sleep reduces that inflammatory burden.
Sleep has long been linked to immune function, but researchers discovered that getting enough of it influenced the environment where monocytes – a type of white blood cell – form, develop, and get primed to support immune function.
This process, hematopoiesis, occurs in the bone marrow.
To assess these mechanisms, researchers studied associations between sleep and monocyte production in humans and mice, which expanded on findings from prior mathematical models.
They analyzed how sleep disruptions increased circulating levels of these immune cells and changed the environment in the bone marrow.
Sleep interruption restructures the epigenome of hematopoietic stem and progenitor cells (HSPCs) and increases their proliferation, thus reducing hematopoietic clonal diversity through accelerated genetic drift.
Sleep fragmentation exerts a lasting influence on the HSPC epigenome, skewing commitment toward a myeloid fate and priming cells for exaggerated inflammatory bursts.
Combining hematopoietic clonal tracking with mathematical modeling, we infer that sleep preserves clonal diversity by limiting neutral drift.
In humans, sleep restriction alters the HSPC epigenome and activates hematopoiesis.
These findings show that sleep slows decay of the hematopoietic system by calibrating the hematopoietic epigenome, constraining inflammatory output, and maintaining clonal diversity.
Getting a consistent good night’s sleep supports normal production and programming of hematopoietic stem cells, a building block of the body’s innate immune system, according to a small National Institutes of Health-supported study in humans and mice.
In a collaborative study led by Marie-Pierre St-Onge, Ph.D., at Columbia University, New York City, 14 adults enrolled in the clinical research trial.
They each participated in a six-week study arm that emulated getting enough sleep (about 7.5 hours each night) or that created sleep deficiency.
To model sleep restriction, adults reduced their nighttime sleep by 1.5 hours – getting about 6 hours of sleep each night.
Sleep conditions were separated by a six-week “washout” period, during which participants returned to their normal sleep patterns.
Morning and afternoon blood samples were collected during the fifth and sixth weeks for each sleep condition.
Researchers found that when adults didn’t get enough sleep, they had higher levels of circulating monocytes in the afternoon.
They also had higher numbers of immune stem cells in the blood and evidence of immune activation.
“The stem cells have been imprinted, or genetically altered, under the influence of sleep restriction,” Swirski said. “The change isn’t permanent, but they continue to self-replicate at a higher rate for weeks.”
A higher production of immune cells creates a more homogenous immune environment, which can accelerate clonal hematopoiesis, an age-related condition that has been linked to increased risks for cardiovascular disease.
Prior studies have identified genetic mutations that drive the proliferation of hematopoietic stem cells.
For more information
Journal of Experimental Medicine
Sleep exerts lasting effects on hematopoietic stem cell function and diversity (September 21 2022)
National Heart, Lung, and Blood Institute (NHLBI)
National Institutes of Health (NIH)
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