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首页> 外文期刊>American Journal of Physiology >Phagocyte migration and cellular stress induced in liver, lung, and intestine during sleep loss and sleep recovery
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Phagocyte migration and cellular stress induced in liver, lung, and intestine during sleep loss and sleep recovery

机译：睡眠丧失和睡眠恢复期间在肝，肺和肠中诱导的吞噬细胞迁移和细胞应激

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Phagocyte migration and cellular stress induced in liver, lung, and intestine during sleep loss and sleep recovery. Am J Physiol Regul Integr Comp Physiol 295: R2067-R2074, 2008. First published October 22, 2008; doi:10.1152/ajpregu.90623.2008.-Sleep is understood to possess recuperative properties and, conversely, sleep loss is associated with disease and shortened life span. Despite these critical attributes, the mechanisms and functions by which sleep and sleep loss impact health still are speculative. One of the most consistent, if largely overlooked, signs of sleep loss in both humans and laboratory rats is a progressive increase in circulating phagocytic cells, mainly neutrophils. The destination, if any, of the increased circulating populations has been unknown and, therefore, its medical significance has been uncertain. The purpose of the present experiment was to determine the content and location of neutrophils in liver and lung tissue of sleep-deprived rats. These are two principal sites affected by neutrophil migration during systemic inflammatory illness. The content of neutrophils in the intestine also was determined. Sleep deprivation in rats was produced for 5 and 10 days by the Bergmann-Rechtschaffen disk method, which has been validated for its high selectivity under freely moving conditions and which was tolerated and accompanied by a deep negative energy balance. Comparison groups included basal conditions and 48 h of sleep recovery after 10 days of sleep loss. Myeloperoxidase (MPO), an enzyme constituent of neutrophils, was extracted from liver, lung, and intestinal tissues, and its activity was determined by spectrophotometry. Leukocytes were located in vasculature and interstitial spaces in the liver and the lung by immunohistochernistry. Heme oxygenase-1, also known as heat shock protein-32 and a marker of cellular stress, and corticosterone also were measured. The results indicate neutrophil migration into extravascular liver and lung tissue concurrent with cell stress and consistent with tissue injury or infection induced by sleep loss. Plasma corticosterone was unchanged. Recovery sleep was marked by increased lung heme oxygenase-1, increased intestinal MPO activity, and abnormally low corticosterone, suggesting ongoing reactive processes as a result of prior sleep deprivation
机译：失眠和睡眠恢复期间在肝，肺和肠中诱导的吞噬细胞迁移和细胞应激。 Am J Physiol Regul Integr Comp Physiol 295：R2067-R2074，2008年。2008年10月22日首次发布; doi：10.1152 / ajpregu.90623.2008.-睡眠被认为具有调理作用，相反，睡眠不足与疾病和寿命缩短有关。尽管具有这些关键属性，但睡眠和失眠影响健康的机制和功能仍是推测性的。在人类和实验室大鼠中，最一致的（即使在很大程度上被忽略）睡眠丧失的迹象之一是循环吞噬细胞（主要是嗜中性粒细胞）的逐渐增加。增加的流动人口的目的地（如果有的话）是未知的，因此其医学意义还不确定。本实验的目的是确定睡眠剥夺大鼠肝脏和肺组织中嗜中性粒细胞的含量和位置。这是系统性炎性疾病期间受嗜中性粒细胞迁移影响的两个主要部位。还测定了肠中嗜中性粒细胞的含量。大鼠的睡眠剥夺通过Bergmann-Rechtschaffen盘法产生了5天和10天，该方法已被证明在自由移动条件下具有高选择性，并且可以忍受并伴有深的负能量平衡。对照组包括基础状况和失眠10天后48小时的睡眠恢复。从肝，肺和肠组织中提取中性粒细胞的一种酶，髓过氧化物酶（MPO），并通过分光光度法测定其活性。通过免疫组织化学将白细胞定位在肝和肺的脉管系统和间质空间中。还测定了血红素加氧酶-1（也称为热休克蛋白-32）和细胞应激的标志物以及皮质酮。结果表明嗜中性粒细胞迁移到血管外的肝和肺组织中并伴有细胞应激，并与睡眠丧失引起的组织损伤或感染相一致。血浆皮质酮未改变。恢复睡眠的特点是肺血红素加氧酶-1增加，肠道MPO活性增加以及皮质酮异常低，这表明由于先前的睡眠不足导致正在进行的反应过程

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