Sleep strongly impacts both humoral and cellular immunity; however, its acute effects on the innate immune defense against pathogens are unclear. Here, we elucidated in mice whether sleep affects the numbers and functions of innate immune cells and their defense against systemic bacterial infection. Sleep significantly increased numbers of classical monocytes in blood and spleen of mice that were allowed to sleep for six hours at the beginning of the normal resting phase compared to mice kept awake for the same time. The sleep-induced effect on classical monocytes was neither caused by alterations in corticosterone nor myelopoiesis, bone marrow egress or death of monocytes and did only partially involve Gαi-protein coupled receptors like chemokine receptor 2 (CCR2), but not the adhesion molecules intercellular adhesion molecule 1 (ICAM-1) or lymphocyte function-associated antigen 1 (LFA-1). Notably, sleep suppressed the expression of the clock gene Arntl in splenic monocytes and the sleep-induced increase in circulating classical monocytes was abrogated in Arntl-deficient animals, indicating that sleep is a prerequisite for clock-gene driven rhythmic trafficking of classical monocytes. Sleep also enhanced the production of reactive oxygen species by monocytes and neutrophils. Moreover, sleep profoundly reduced bacterial load in blood and spleen of mice that were allowed to sleep before systemic bacterial infection and consequently increased survival upon infection. These data provide the first evidence that sleep enhances numbers and function of innate immune cells and therewith strengthens early defense against bacterial pathogens.

中文翻译：

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睡眠增强单核细胞的数量和功能并改善小鼠的细菌感染结果

睡眠强烈影响体液免疫和细胞免疫；然而，其对病原体的先天免疫防御的急性影响尚不清楚。在这里，我们在小鼠身上阐明了睡眠是否会影响先天免疫细胞的数量和功能以及它们对全身细菌感染的防御。与同时保持清醒的小鼠相比，睡眠显着增加了在正常休息阶段开始时允许睡眠 6 小时的小鼠血液和脾脏中经典单核细胞的数量。对经典单核细胞的睡眠诱导作用既不是由皮质酮的改变也不是由骨髓生成、骨髓流出或单核细胞的死亡引起的，并且仅部分涉及 Gαi 蛋白偶联受体，如趋化因子受体 2 (CCR2)，但不是粘附分子细胞间粘附分子 1 (ICAM-1) 或淋巴细胞功能相关抗原 1 (LFA-1)。值得注意的是，睡眠抑制了脾单核细胞中时钟基因 Arntl 的表达，并且在 Arntl 缺陷的动物中睡眠诱导的循环经典单核细胞增加被废除，表明睡眠是时钟基因驱动的经典单核细胞有节奏的运输的先决条件。睡眠还增强了单核细胞和中性粒细胞产生的活性氧。此外，睡眠显着降低了在全身细菌感染前睡眠的小鼠血液和脾脏中的细菌负荷，从而增加了感染后的存活率。