Cousins Center for Psychoneuroimmunology, UCLA Semel Institute, 300 Medical Plaza, Los Angeles, CA 90095-7057, USA.
Ann Behav Med. 2011 Oct;42(2):141-52. doi: 10.1007/s12160-011-9280-2.
Poor sleep is prospectively linked to all-cause and cardiovascular mortality. Inflammatory processes may be an important biological mechanism linking poor sleep to cardiovascular disease. Such processes involve active participation of signaling molecules called cytokines in development of atherosclerotic plaques.
I review evidence from experimental sleep deprivation and clinical observational studies suggesting a bidirectional relationship between sleep and inflammatory cytokines.
Findings from sleep deprivation studies indicate that sleep loss is associated with increases in these cytokines. Similarly, studies in clinical populations with sleep problems, such as primary insomnia patients and those diagnosed with major depression, also show elevations in these same cytokines.
Bidirectional communication between the brain and the immune system is carried out through a complex network of autonomic nerves, endocrine hormones, and cytokines. Disturbed sleep appears to perturb the functioning of this network and therefore contribute to elevations in inflammatory mediators linked to cardiovascular disease.
睡眠质量差与全因死亡率和心血管死亡率都呈正相关。炎症过程可能是将睡眠质量差与心血管疾病联系起来的一个重要生物学机制。在动脉粥样硬化斑块的发展过程中，这些炎症过程涉及到信号分子（称为细胞因子）的积极参与。
我回顾了实验性睡眠剥夺和临床观察性研究的证据，这些研究表明睡眠和炎症细胞因子之间存在双向关系。
睡眠剥夺研究的结果表明，睡眠不足与这些细胞因子的增加有关。同样，在有睡眠问题的临床人群中进行的研究，如原发性失眠患者和被诊断患有重度抑郁症的患者，也显示出这些相同细胞因子的升高。
大脑和免疫系统之间的双向通讯是通过自主神经系统、内分泌激素和细胞因子的复杂网络进行的。睡眠紊乱似乎扰乱了这个网络的功能，因此导致与心血管疾病相关的炎症介质升高。
