Schuld A, Mullington J, Hermann D, Hinze-Selch D, Fenzel T, Holsboer F, Pollmächer T
Max Planck Institute of Psychiatry, D-80804 Munich, Germany.
Am J Physiol. 1999 Apr;276(4):R1149-55. doi: 10.1152/ajpregu.1999.276.4.R1149.
Numerous animal studies suggest that cytokines such as interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) mediate increased sleep amount and intensity observed during infection and are, moreover, involved in physiological sleep regulation. In humans the role of cytokines in sleep-wake regulation is largely unknown. In a single-blind, placebo-controlled study, we investigated the effects of granulocyte colony-stimulating factor (G-CSF, 300 microgram sc) on the plasma levels of cytokines, soluble cytokine receptors, and hormones as well as on night sleep. G-CSF did not affect rectal temperature or the plasma levels of cortisol and growth hormone but did induce increases in the plasma levels of IL-1 receptor antagonist and both soluble TNF receptors within 2 h after injection. In parallel, the amount of slow-wave sleep and electroencephalographic delta power were reduced, indicating a lowered sleep intensity. We conclude that G-CSF suppresses sleep intensity via increased circulating amounts of endogenous antagonists of IL-1beta and TNF-alpha activity, suggesting that these cytokines are involved in human sleep regulation.
大量动物研究表明，诸如白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）等细胞因子介导了感染期间观察到的睡眠时间增加和睡眠强度增强，此外，还参与生理睡眠调节。在人类中，细胞因子在睡眠-觉醒调节中的作用很大程度上未知。在一项单盲、安慰剂对照研究中，我们研究了粒细胞集落刺激因子（G-CSF，300微克皮下注射）对细胞因子、可溶性细胞因子受体和激素的血浆水平以及夜间睡眠的影响。G-CSF不影响直肠温度或皮质醇和生长激素的血浆水平，但在注射后2小时内确实诱导了IL-1受体拮抗剂和两种可溶性TNF受体的血浆水平升高。同时，慢波睡眠量和脑电图δ波功率降低，表明睡眠强度降低。我们得出结论，G-CSF通过增加循环中IL-1β和TNF-α活性的内源性拮抗剂量来抑制睡眠强度，这表明这些细胞因子参与人类睡眠调节。
