Sleep enhances IL-6 trans-signaling in humans

Dimitrov, Stoyan, Lange, Tanja, Benedict, Christian, Nowell, Mari Ann, Jones, Simon Arnett ORCID: https://orcid.org/0000-0001-7297-9711, Scheller, Jurgen, Rose-John, Stefan and Born, Jan 2006. Sleep enhances IL-6 trans-signaling in humans. The FASEB Journal 20 (12) , pp. 2174-2176. 10.1096/fj.06-5754fje

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Abstract

Sleep is commonly considered to support immune defense. The underlying sleep-immune interaction appears to rely critically on cytokines, like interleukin-6 (IL-6), that combine effects on immune and neuronal functions. The IL-6 signal is conveyed in two ways: it stimulates a restricted group of (mostly immune) cells via membrane-bound IL-6 receptors (mIL-6R) by forming a complex with soluble IL-6R (sIL-6R), and it stimulates (via membrane-bound gp130) a great variety of other cell types--a process termed trans-signaling. Focusing on the receptor side of IL-6 signaling, we examined the effect of sleep on sIL-6R plasma concentrations, mIL-6R expression, plasma sgp130, and numbers of IL-6-producing monocytes in healthy humans who were tested during a regular sleep-wake cycle and 24 h of wakefulness while blood was sampled repeatedly. Sleep strongly enhanced concentrations of sIL-6R, exceeding wake levels by 70% at the end of sleep. This rise was due to an increase in the PC (proteolytic cleavage) rather than the DS (differentially spliced) variant of sIL-6R. Sleep did not affect IL-6-producing monocytes, mIL-6R density, or sgp130 concentrations. The selective increase in sIL-6R implicates an enhanced trans-signaling capacity whereby sleep distinctly widens the profile of IL-6 actions, enabling an integrated influence on brain and peripheral organs.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Medicine Systems Immunity Research Institute (SIURI)
Publisher:	Federation of American Society of Experimental Biology
ISSN:	0892-6638
Last Modified:	06 Nov 2024 22:34
URI:	https://orca.cardiff.ac.uk/id/eprint/224

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