Numerous animal studies suggest that cytokines such as interleukin-1 (IL-1) and tumor necrosis factor- (TNF-) 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 µg 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-1 and TNF- activity, suggesting that these cytokines are involved in human sleep regulation.

tumor necrosis factor-; interleukin-1; soluble tumor necrosis factor receptors; interleukin-1 receptor antagonist; non-rapid eye movement sleep

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