Abstract
A reduction in the amount of time spent sleeping occurs chronically in modern society. Clinical and experimental studies in humans and animal models have shown that immune function is impaired when sleep loss is experienced. Sleep loss exerts a strong regulatory influence on peripheral levels of inflammatory mediators of the immune response. An increasing number of research projects support the existence of reciprocal regulation between sleep and low-intensity inflammatory response. Recent studies show that sleep deficient humans and rodents exhibit a proinflammatory component; therefore, sleep loss is considered as a risk factor for developing cardiovascular, metabolic, and neurodegenerative diseases (e.g., diabetes, Alzheimer's disease, and multiple sclerosis). Circulating levels of proinflammatory mediators depend on the intensity and duration of the method employed to induce sleep loss. Recognizing the fact that the concentration of proinflammatory mediators is different between acute and chronic sleep-loss may expand the understanding of the relationship between sleep and the immune response. The aim of this review is to integrate data from recent published reports (2002–2013) on the effects of sleep loss on the immune response. This review may allow readers to have an integrated view of the mechanisms involved in central and peripheral deficits induced by sleep loss.
Highlights
Sleep is a vital phenomenon, classically divided into two distinct phases: sleep with rapid eye movements (REM) and sleep without rapid eye movements [1]
Because IL-1α, IL1β, and TNF-α are the most studied cytokines involved in sleep regulation, we focus mainly on these three cytokines; the role of IL-6 will be reviewed because this proinflammatory cytokine is highly related to the interaction between sleep loss and the immune response
We reported that chronic REM sleep restriction in rats induces blood-brain barrier disruption and that brief sleep recovery periods lessened these effects in several brain regions
Summary
Sleep is a vital phenomenon, classically divided into two distinct phases: sleep with rapid eye movements (REM) and sleep without rapid eye movements (non-REM) [1]. REM sleep is characterized by EEG activity similar to that of waking and by the loss of muscle tone [2, 3] Both phases, REM sleep and non-REM sleep, alternate throughout total sleep time [2, 3]. Sleep loss effects can be evaluated by several methodologies, including acute total or selective sleep deprivation and sleep restriction ( called partial sleep deprivation) or sleep fragmentation. The majority of animal models used to study the physiological effects of sleep loss are based primarily on total sleep deprivation [16]. This method does not resemble human conditions, it still provides valuable information on sleep loss effects. We propose how sleep recovery might restore the normal balance between proinflammatory and anti-inflammatory molecules at the systemic level and how immune mediators might be in direct contact with the central nervous system via blood-brain barrier disruption, modifying neural activity and the possible pathway for neurological impairments
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