Phagocyte migration and cellular stress induced in liver, lung, and intestine during sleep loss and sleep recovery
Phagocyte migration and cellular stress induced in liver, lung, and intestine during sleep loss and sleep recovery
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DOI：
10.1152/ajpregu.90623.2008
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发表时间：
2008-12-01
影响因子：
2.8
通讯作者：
Hogg, Neil
中科院分区：
文献类型：
--
作者：
Everson, Carol A.;Thalacker, Christa D.;Hogg, Neil
王志刚，王志刚，王志刚，等。睡眠缺失和睡眠恢复过程中肝、肺和肠道中白细胞迁移和细胞应激的影响。[J] .中国生物医学工程学报，2016,33(4):557 - 557。首次发表于2008年10月22日；doi: 10.1152 / ajpregu.90623.2008。睡眠被认为具有恢复的特性，相反，睡眠不足与疾病和寿命缩短有关。尽管有这些关键的属性，睡眠和睡眠不足影响健康的机制和功能仍然是推测性的。在人类和实验室大鼠中，睡眠不足的一个最一致的迹象是循环吞噬细胞（主要是中性粒细胞）的逐渐增加，这在很大程度上被忽视了。增加的流动人口的目的地（如果有的话）是未知的，因此其医学意义是不确定的。本实验的目的是测定睡眠剥夺大鼠肝脏和肺组织中中性粒细胞的含量和位置。这是在全身性炎症疾病中受中性粒细胞迁移影响的两个主要部位。同时测定了肠道中性粒细胞的含量。采用Bergmann-Rechtschaffen圆盘法对大鼠进行5天和10天的睡眠剥夺，该方法在自由运动条件下具有高选择性，并且具有耐受性并伴有深度负能量平衡。对照组包括基础条件组和睡眠不足10天后的48小时睡眠恢复组。髓过氧化物酶（MPO）是中性粒细胞的一种组成酶，从肝、肺和肠组织中提取，并用分光光度法测定其活性。免疫组化法发现白细胞分布于肝、肺的血管和间质。血红素加氧酶-1，也被称为热休克蛋白-32，是细胞应激的标志，皮质酮也被测量。结果表明，中性粒细胞向血管外肝脏和肺组织的迁移与细胞应激同时发生，与睡眠不足引起的组织损伤或感染一致。血浆皮质酮水平不变。恢复性睡眠的特征是肺血红素加氧酶-1增加，肠道MPO活性增加，皮质酮异常低，表明先前睡眠剥夺导致持续的反应过程。
Everson CA, Thalacker CD, Hogg N. 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 immunohistochemistry. 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.