Sleep loss activates cellular inflammation and signal transducer and activator of transcription (STAT) family proteins in humans.
Sleep loss activates cellular inflammation and signal transducer and activator of transcription (STAT) family proteins in humans.
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DOI：
10.1016/j.bbi.2014.09.017
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发表时间：
2015-07
影响因子：
15.1
通讯作者：
Breen, Elizabeth Crabb
中科院分区：
文献类型：
--
作者：
Irwin, Michael R.;Witarama, Tuff;Caudill, Marissa;Olmstead, Richard;Breen, Elizabeth Crabb
关键词：
睡眠障碍和睡眠时间短与炎症和相关疾病有关，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丧失对自发性细胞炎症以及信号转导和转录激活因子（STAT）家族蛋白的激活的影响，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，在不间断基线睡眠、部分睡眠剥夺（PSD，睡眠时间为3 a.m.至7 a.m.）恢复睡眠。与基线相比，PSD后（P<0.02）和恢复睡眠后（P<0.01）单核细胞自发表达IL-6和TNF-α的水平显著升高。与基线相比，在恢复睡眠后，活化的STAT 1和STAT 5的自发单核细胞表达显著增加（分别为P<0.007和P <0.02），但STAT 3的自发单核细胞表达没有增加（P=0.09）。在淋巴细胞群中未发现STAT 1、STAT 3或STAT 5的变化。睡眠丧失诱导自发性细胞先天免疫和STAT家族蛋白的激活，它们一起将睡眠丧失的动力学映射到调节炎症和其他免疫应答的分子信号传导途径上。针对短睡眠时间的治疗有可能抑制炎症并降低人类炎症性疾病和某些癌症的风险。
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 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 3 a.m. to 7 a.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 STAT 1 and STAT 5 was significantly greater after recovery sleep (P<0.007P<0.02, respectively) but not STAT 3 (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.
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影响因子：
6.1
作者：
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睡眠损失激活炎症的细胞标记：性别差异。
影响因子：
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