title: Sleep and innate immunity.
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.
authors.affiliation: Sleep and Performance Research Center, Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman, WA 99164-6520, USA.
authors.forename: Mark R
authors.initials: MR
authors.lastname: Zielinski
authors.forename: James M
authors.initials: JM
authors.lastname: Krueger
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism*; D054884:Host-Pathogen Interactions / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology*; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism; D009457:Neuroglia / Q000378:metabolism*; D051192:Receptors, Pattern Recognition / Q000378:metabolism; D012890:Sleep / Q000276:immunology* / Q000502:physiology
chemical_list: D016207:Cytokines; D051192:Receptors, Pattern Recognition; D000255:Adenosine Triphosphate