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Sleep and Immune Regulation - Sleep It Off?

What is the relationship between sleep and our immune system? In a fantastic new review of the subject by Dr. Michael Irwin, MD (Professor of Psychiatry and Behavioral Sciences, Professor of Psychology, and Director of the Cousins Center for Psychoneuroimmunology at the Semel Institute for Neuroscience), the beneficial crosstalk between sleep and host defense mechanisms is explored, as are the potential host-immune consequences that may result from misalignment of the two.

Although sleep is a period of low metabolic demand, it is thought that sleep mediates a host defense response to pathogens during this period of quiescence – preparing the body for the day ahead. Studies have shown that nocturnal sleep seems to be necessary for the nocturnal increases in systemic levels of the cytokine IL-6 (which has a circadian profile, peaking in the evening and early morning hours). Experimental sleep deprivation induces an under-secretion of IL-6 at night, and attenuates monocyte production of cytokines during the night.

Naturally occurring sleep and slow wave sleep are associated with increases in antiviral immune response profiles, and enhance the expression of immune markers implicated in immune defense. Acute sleep disturbance shifts the transcriptional profile towards increased inflammatory activity and decreased antiviral responses which might result in poor vaccine responses and increased susceptibility to infectious diseases. Moreover, during sleep disturbance, activation of the sympathetic nervous system (SNS) leads to the release of noradrenaline, resulting in the suppressed transcription of antiviral immune response genes, but enhanced transcription of inflammatory immune response genes. Additionally, chronic sleep deprivation leads to sustained activation of the hypothalamic pituitary axis, reduced glucocorticoid sensitivity, and increases in SNS outflow. This too may steer the immune system toward a pro-inflammatory profile and away from an antiviral profile.

Additionally, the review also describes the inverse relationship - the influence of inflammation on sleep itself. When the innate immune system is activated in response to stress at a cellular level or infectious challenge, inflammatory cytokines are released, which together signal the central nervous system (CNS) to promote increased sleep duration and slow wave sleep. These changes might facilitate the development of immune memory, although experimental support for this is limited. On the other hand, chronic inflammatory disorders or high levels of inflammation seem to decrease sleep duration, induce sleep fragmentation and increase REM sleep, with reciprocal loss of slow wave sleep.

Overall, this review nicely outlines the relationship between normal sleep and immune regulation, as well as acute and chronic sleep deprivation and their potential immunomodulatory effects. Further research is needed to understand the possible therapeutic potential of sleep to mitigate the risk of inflammatory and infectious diseases. Until then, I guess the old saying does hold some truth: "Sleep it off!"