Sleep and Inflammation: Psychoneuroimmunology in the Context of Cardiovascular Disease
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ORIGINAL ARTICLE
Sleep and Inflammation: Psychoneuroimmunology in the Context of Cardiovascular Disease Sarosh J. Motivala, Ph.D.
Published online: 21 May 2011 # The Society of Behavioral Medicine 2011
Abstract Background Poor sleep is prospectively linked to all-cause and cardiovascular mortality. Inflammatory processes may be an important biological mechanism linking poor sleep to cardiovascular disease. Such processes involve active participation of signaling molecules called cytokines in development of atherosclerotic plaques. Purpose I review evidence from experimental sleep deprivation and clinical observational studies suggesting a bidirectional relationship between sleep and inflammatory cytokines. Results Findings from sleep deprivation studies indicate that sleep loss is associated with increases in these cytokines. Similarly, studies in clinical populations with sleep problems, such as primary insomnia patients and those diagnosed with major depression, also show elevations in these same cytokines. Conclusions Bidirectional communication between the brain and the immune system is carried out through a complex network of autonomic nerves, endocrine hormones, and cytokines. Disturbed sleep appears to perturb the functioning of this network and therefore contribute to elevations in inflammatory mediators linked to cardiovascular disease. Keywords Sleep . Inflammation . Cytokines . Insomnia . Cardiovascular disease . Psychoneuroimmunology
Introduction Inflammare loosely translates from Latin as “to set on fire,” which fittingly characterizes the potential of chronic inflammation to cause harm [1]. Inflammation is coordinated through the immune system, with leukocytes, cells of the immune system, relying on signaling molecules termed cytokines to communicate and coordinate inflammatory processes. In addition to the immune system, adipose and muscle tissue are also sources of inflammatory cytokines [2]. Chronic activation of inflammatory processes is thought to drive atherosclerosis and promote cardiovascular disease. Although acute inflammation can be thought of as a short-lasting, highly localized process, chronic inflammation is different, involving elevations in systemic circulating levels of inflammatory makers such as C-reactive protein (CRP) and interleukin-6 (IL-6), increased production of inflammatory cytokines by immune cells and within these immune cells, and increased gene transcription of inflammatory cytokines [1, 3, 4]. Systemic levels of inflammatory cytokines communicate distally with the brain, and the magnitude, extent, and nature of leukocyte action can be modified by the brain via autonomic nerves and neuroendocrine hormones [5–7]. It is through these pathways that poor sleep can influence inflammatory cytokines [8–10] and conversely through which the immune system, via these same cytokines, can affect sleep [11] (Fig. 1).
Characterizing Poor Sleep S. J. Motivala (*) Cousins Center for Psychoneuroimmunology, UCLA Semel Institute, 300 Medical Plaza, Room 3153, Los Angeles, CA 90095-7057,
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