Journal article
Sleep and innate immunity
Frontiers in bioscience (Scholar edition), Vol.3, pp.632-642
01/01/2011
Handle:
https://hdl.handle.net/2376/110132
PMCID: PMC3645929
PMID: 21196401
Abstract
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.
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Details
- Title
- Sleep and innate immunity
- Creators
- Mark R Zielinski - Sleep and Performance Research Center, Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman, WA 99164-6520, USAJames M Krueger
- Publication Details
- Frontiers in bioscience (Scholar edition), Vol.3, pp.632-642
- Academic Unit
- Integrative Physiology and Neuroscience, Department of
- Publisher
- United States
- Grant note
- R01 NS025378 / NINDS NIH HHS NS25378 / NINDS NIH HHS R01 NS031453 / NINDS NIH HHS NS31453 / NINDS NIH HHS R01 HD036520 / NICHD NIH HHS HD36520 / NICHD NIH HHS
- Identifiers
- 99900547151101842
- Language
- English
- Resource Type
- Journal article