Sleep loss as a factor to induce cellular and molecular inflammatory variations

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.

Figure 1

Sleep loss promotes a low-grade proinflammatory status. Sleep loss is characterized by an increase in circulating proinflammatory cytokines (IL-1β, IL-6, IL-17A, TNF-α) and CRP. Image shows the differential effect of sleep loss on the immune system after acute total sleep deprivation and prolonged sleep restriction and or sleep fragmentation. The acute and chronic events of sleep loss correlate with the temporal immune response (innate and adaptive). Prolonged sleep loss plus insufficient sleep recovery are considered an important risk factor to develop metabolic, cardiovascular, and neurodegenerative diseases related with the deregulation of the neuro-endocrine-immune network. Abbreviations: APCs; antigen-presenting cells; CRP, C-reactive protein; CVD, cardiovascular disease; N, neurodegenerative diseases; NK, natural killer; SR, sleep restriction; SF, sleep fragmentation; TSD, total sleep deprivation.