Better together: Sleep, circadian genes, and immunity.
Better together: Sleep, circadian genes, and immunity.
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更好的结合：睡眠、昼夜节律基因和免疫力。
DOI：
10.1016/j.bbi.2020.04.011
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发表时间：
2020
期刊：
影响因子：
--
通讯作者：
Prather,AricA
中科院分区：
文献类型：
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作者：
Prather,AricA
睡眠对于维持身体健康至关重要，缺乏充足的睡眠会导致各种疾病的风险增加，包括容易受到感染。事实上，早期对大鼠的研究表明，长期实验性睡眠不足会导致宿主抵抗力严重崩溃，并随后因败血症而死亡[1]。在横断面、前瞻性和实验研究中，人类睡眠不足，例如每晚睡眠少于 6 小时，与感染性疾病的易感性增加有关 [2],[3],[4]。迄今为止，许多与睡眠和传染病相关的研究都集中在病毒感染和适应性免疫功能的作用上，而对先天免疫的关注较少。 Hahn 及其同事的研究 [5] 通过调查睡眠依赖性对循环单核细胞数量和功能的影响扩展了后一个研究领域，循环单核细胞是吞噬细胞，对于防止细菌感染至关重要。 在这项研究中，通过温和的处理，小鼠经历了 6 小时的睡眠不足，并与允许不受干扰地睡眠的小鼠进行了比较。与睡眠不足的小鼠相比，未受干扰的小鼠外周血和脾脏中的经典单核细胞 (Ly6C hi CD11b+ CD115+) 升高，而多形核 (PMN) 细胞则没有观察到一致的差异。随后的分析和实验证实，睡眠相关的单核细胞增加并不是由于睡眠剥夺小鼠中细胞过度死亡或从单核细胞向巨噬细胞的更大分化，也不是由于睡眠小鼠中骨髓生成或单核细胞从骨髓中迁移的上调。相反，这些增加部分依赖于 CCR2 趋化因子信号传导。然而，也许最有趣的是发现 BMAL1 缺陷小鼠中循环单核细胞的群体差异被消除，这突显了昼夜节律系统在调节睡眠期间单核细胞重新分布中的作用。
Sleep is vital to maintaining physical health, and a lack of adequate sleep can lead to increased risk for a variety of medical conditions, including vulnerability to infections. Indeed, early work in rats showed that prolonged experimental sleep loss produced profound breakdowns in host resistance and subsequent death due to septicemia [1]. In humans, insufficient sleep, eg, sleeping fewer than 6 h per night, has been associated with increased susceptibility to infectious illness in cross-sectional, prospective, and experimental studies [2],[3],[4]. To date, much of the research related to sleep and infectious illness has focused on viral infections and the role of adaptive immune function, with less attention paid to innate immunity. The study by Hahn and colleagues [5] extends this latter research area by investigating the sleep dependent influences on number and function of circulating monocytes, which are phagocytes critical to protection against bacterial infections.In this study, mice were subjected to 6 h of sleep loss, via gentle handling, and compared to mice who were allowed to sleep undisturbed. Compared to mice exposed to sleep loss, the undisturbed mice displayed elevations in classical monocytes (Ly6C hi CD11b+ CD115+) in peripheral blood and in the spleen, while there were no consistent differences observed with respect to polymorphonuclear (PMN) cells. Subsequent analyses and experiments confirmed that the sleep related increases in monocytes were not due to excess cell death or greater differentiation from monocytes to macrophages among sleep deprived mice, or an upregulation in myelopoiesis or migration of monocytes from the bone marrow in sleeping mice. Rather, these increases were partially dependent of CCR2 chemokine signaling. Perhaps most intriguing, however, was the finding that group differences in circulating monocytes were abrogated in BMAL1 deficient mice, highlighting the role of the circadian system in regulating the redistribution of monocytes during sleep.