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Am J Physiol Regul Integr Comp Physiol 278: R947-R955, 2000;
0363-6119/00 $5.00
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Vol. 278, Issue 4, R947-R955, April 2000

Dose-dependent effects of endotoxin on human sleep

Janet Mullington, Carsten Korth, Dirk M. Hermann, Armin Orth, Chris Galanos, Florian Holsboer, and Thomas Pollmächer

Max Planck Institute of Psychiatry, Clinical Institute, Munich, Germany D-80804

The role of the central nervous system in the host response to infection and inflammation and modulation of these responses by the hypothalamic-pituitary-adrenal system are well established. In animals, activation of host defense mechanisms increases non-rapid eye movement (NREM) sleep amount and intensity, which, in turn, are thought to support host defense, or the body's ability to defend itself against challenges to its immune system. In humans, the evidence is conflicting. Therefore, we investigated the effects of three placebo-controlled doses of endotoxin on host response, including nocturnal sleep in healthy volunteers. Administered before nocturnal sleep onset, endotoxin dose dependently increased rectal temperature, heart rate, and the plasma levels of tumor necrosis factor (TNF)-alpha , soluble TNF receptors, interleukin (IL)-1 receptor antagonist, IL-6, and cortisol. The lowest dose reliably increased circulating levels of cytokines and soluble cytokine receptors, but it did not affect rectal temperature, heart rate, or cortisol. This subtle host defense activation increased deep NREM sleep amount, often referred to as slow-wave sleep (stages 3 and 4), and intensity (delta power). Conversely, the highest dose of endotoxin disrupted sleep. Whereas it is well established that the endocrine and thermoregulatory systems are very sensitive to endotoxin, this study shows that human sleep-wake behavior is even more sensitive to activation of host defense mechanisms.

tumor necrosis factor; interleukin-6; interleukin-1 receptor antagonist; cortisol; fever; inflammation; cytokines; cytokine receptors; lipopolysaccharide


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