睡眠与先天免疫。
Sleep and innate immunity.
作者信息
Zielinski Mark R, Krueger James M
机构信息
Sleep and Performance Research Center, Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman, WA 99164-6520, USA.
出版信息
Front Biosci (Schol Ed). 2011 Jan 1;3(2):632-42. doi: 10.2741/s176.
Many pro-inflammatory molecules, such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) are somnogenic, while many anti-inflammatory molecules inhibit sleep. Sleep loss increases the production/release of these sleep regulatory pro-inflammatory molecules. Further, sleep changes occurring during various pathologies are mediated by these inflammatory substances in response to pathogen recognition and subsequent inflammatory cellular pathways. This review summarizes information and concepts regarding inflammatory mechanisms of the innate immune system that mediate sleep. Further, we discuss sleep-immune interactions in regards to sleep in general, pathologies, and sleep as a local phenomenon including the central role that extracellular ATP plays in the initiation of sleep.
许多促炎分子，如白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）具有促眠作用，而许多抗炎分子则抑制睡眠。睡眠不足会增加这些睡眠调节促炎分子的产生/释放。此外，在各种病理过程中发生的睡眠变化是由这些炎症物质介导的，以响应病原体识别和随后的炎症细胞途径。本综述总结了关于介导睡眠的先天性免疫系统炎症机制的信息和概念。此外，我们还讨论了一般睡眠、病理状态下的睡眠-免疫相互作用，以及作为局部现象的睡眠，包括细胞外ATP在睡眠起始中所起的核心作用。
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