Irwin Michael R, Witarama Tuff, Caudill Marissa, Olmstead Richard, Breen Elizabeth Crabb
University of California, Los Angeles - Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, United States.
University of California, Los Angeles - Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, United States.
Brain Behav Immun. 2015 Jul;47:86-92. doi: 10.1016/j.bbi.2014.09.017. Epub 2014 Oct 17.
Sleep disturbance and short sleep duration are associated with inflammation and related disorders including cardiovascular disease, arthritis, diabetes mellitus, and certain cancers. This study was undertaken to test the effects of experimental sleep loss on spontaneous cellular inflammation and activation of signal transducer and activator of transcription (STAT) family proteins, which together promote an inflammatory microenvironment. In 24 healthy adults (16 females; 8 males), spontaneous production of IL-6 and TNF-α in monocytes and spontaneous intranuclear expression of activated STAT1, STAT3, and STAT5 in peripheral blood mononuclear cells (PBMC), monocyte-, and lymphocyte populations were measured in the morning after uninterrupted baseline sleep, partial sleep deprivation (PSD, sleep period from 3a.m. to 7a.m.), and recovery sleep. Relative to baseline, spontaneous monocytic expression of IL-6 and TNF-α was significantly greater after PSD (P<0.02) and after recovery sleep (P<0.01). Relative to baseline, spontaneous monocytic expression of activated STAT1 and STAT5 was significantly greater after recovery sleep (P<0.007 and P<0.02, respectively) but not STAT3 (P=0.09). No changes in STAT1, STAT3, or STAT5 were found in lymphocyte populations. Sleep loss induces activation of spontaneous cellular innate immunity and of STAT family proteins, which together map the dynamics of sleep loss on the molecular signaling pathways that regulate inflammatory and other immune responses. Treatments that target short sleep duration have the potential to constrain inflammation and reduce the risk for inflammatory disorders and some cancers in humans.
睡眠障碍和短睡眠时间与炎症及相关疾病有关，这些疾病包括心血管疾病、关节炎、糖尿病和某些癌症。本研究旨在测试实验性睡眠剥夺对自发性细胞炎症以及信号转导和转录激活因子（STAT）家族蛋白激活的影响，这些蛋白共同促进炎症微环境。在24名健康成年人（16名女性；8名男性）中，在连续基线睡眠、部分睡眠剥夺（PSD，凌晨3点至7点的睡眠时间）和恢复睡眠后的早晨，测量单核细胞中IL-6和TNF-α的自发产生，以及外周血单核细胞（PBMC）、单核细胞和淋巴细胞群体中活化的STAT1、STAT3和STAT5的自发核内表达。相对于基线，PSD后（P<0.02）和恢复睡眠后（P<0.01），单核细胞中IL-6和TNF-α的自发表达显著增加。相对于基线，恢复睡眠后活化的STAT1和STAT5的单核细胞自发表达显著增加（分别为P<0.007和P<0.02），但STAT3没有增加（P=0.09）。淋巴细胞群体中未发现STAT1、STAT3或STAT5有变化。睡眠剥夺会诱导自发性细胞固有免疫和STAT家族蛋白的激活，它们共同描绘了睡眠剥夺在调节炎症和其他免疫反应的分子信号通路上动态变化。针对短睡眠时间的治疗有可能抑制炎症，并降低人类患炎症性疾病和某些癌症的风险。
