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

Sleep loss as a factor to induce cellular and molecular inflammatory variations.
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DOI:
10.1155/2013/801341
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发表时间:
2013
影响因子:
--
通讯作者:
Gómez-González B
Gómez-González B
中科院分区:
其他
文献类型:
--
作者:
Hurtado-Alvarado G;Pavón L;Castillo-García SA;Hernández ME;Domínguez-Salazar E;Velázquez-Moctezuma J;Gómez-González B

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在现代社会中,睡眠时间的减少是长期存在的。在人类和动物模型上的临床和实验研究表明,当经历睡眠不足时,免疫功能会受到损害。睡眠不足对免疫反应的外周炎症介质水平有很强的调节作用。越来越多的研究项目支持睡眠和低强度炎症反应之间存在相互调节。最近的研究表明,睡眠不足的人类和啮齿动物表现出促炎成分;因此,睡眠不足被认为是发生心血管、代谢和神经退行性疾病(如糖尿病、阿尔茨海默病和多发性硬化症)的危险因素。促炎介质的循环水平取决于诱导失眠的方法的强度和持续时间。认识到急性和慢性睡眠缺失的促炎介质浓度不同这一事实,可能会扩大对睡眠和免疫反应之间关系的理解。这篇综述的目的是整合最近发表的关于睡眠不足对免疫反应影响的报告(2002-2013)的数据。这篇综述可能会让读者对睡眠缺失导致的中枢和外周功能障碍的机制有一个完整的认识。
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.
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