Frey Danielle J, Fleshner Monika, Wright Kenneth P
Sleep and Chronobiology Laboratory, Department of Integrative Physiology, Center for Neuroscience, University of Colorado at Boulder, Clare Small, Room 114, Campus Box 354, Boulder, CO 80309, USA.
Brain Behav Immun. 2007 Nov;21(8):1050-7. doi: 10.1016/j.bbi.2007.04.003. Epub 2007 May 23.
Inflammatory cytokines are released in response to stress, tissue damage, and infection. Acutely, this response is adaptive; however, chronic elevation of inflammatory proteins can contribute to health problems including cardiovascular, endocrine, mood, and sleep disorders. Few studies have examined how sleep deprivation acutely affects inflammatory markers, which was the aim of the current study. Nineteen healthy men and women aged 28.05+/-8.56 (mean+/-SD) were totally sleep deprived for 40 h under constant routine conditions. Pro-inflammatory markers: intracellular adhesion molecule-1 (ICAM-1), E-selectin, vascular adhesion molecule-1 (VCAM-1), c-reactive protein (CRP), interleukin-6 (IL-6), and interleukin-1beta (IL-1beta), and the anti-inflammatory cytokine interleukin-1 receptor antagonist (IL-1ra) were assayed in plasma. Daytime levels during baseline (hours 1-15 of scheduled wakefulness) were compared to daytime levels during sleep deprivation (hours 25-39 of scheduled wakefulness), thus controlling for circadian phase within an individual. Repeated measures ANOVA with planned comparisons showed that 40 h of total sleep deprivation induced a significant increase in E-selectin, ICAM-1, IL-1beta, and IL-1ra, a significant decrease in CRP and IL-6, and no significant change in VCAM-1. Alterations in circulating levels of pro- and anti-inflammatory cytokines and cell adhesion molecules during sleep deprivation were consistent with both increased and decreased inflammation. These findings suggest that one night of sleep loss triggers a stress response that includes stimulation of both pro- and anti-inflammatory proteins in the healthy young subjects tested under our experimental conditions.
炎症细胞因子会因应激、组织损伤和感染而释放。急性情况下,这种反应具有适应性;然而,炎症蛋白的长期升高会导致包括心血管、内分泌、情绪和睡眠障碍在内的健康问题。很少有研究探讨睡眠剥夺如何急性影响炎症标志物,这正是本研究的目的。19名年龄在28.05±8.56(均值±标准差)的健康男性和女性在恒定日常条件下完全睡眠剥夺40小时。检测血浆中的促炎标志物:细胞间黏附分子-1(ICAM-1)、E-选择素、血管黏附分子-1(VCAM-1)、C反应蛋白(CRP)、白细胞介素-6(IL-6)和白细胞介素-1β(IL-1β),以及抗炎细胞因子白细胞介素-1受体拮抗剂(IL-1ra)。将基线期(计划清醒的第1至15小时)的日间水平与睡眠剥夺期(计划清醒的第25至39小时)的日间水平进行比较,从而控制个体内的昼夜节律相位。采用计划比较的重复测量方差分析表明,40小时的完全睡眠剥夺导致E-选择素、ICAM-1、IL-1β和IL-1ra显著增加,CRP和IL-6显著降低,VCAM-1无显著变化。睡眠剥夺期间促炎和抗炎细胞因子及细胞黏附分子循环水平的改变与炎症的增加和减少均一致。这些发现表明,在我们的实验条件下,一晚的睡眠缺失会引发一种应激反应,其中包括对健康年轻受试者体内促炎和抗炎蛋白的刺激。