title: Effects of sleep on endotoxin-induced host responses in healthy men.
abstract: OBJECTIVE
  To examine whether increased sleep during viral or bacterial infections supports host defense mechanisms.
  
  
  METHODS
  To test this assumption in humans, healthy male subjects were assigned either to sleep from 2300 to 0700 hours (n = 10) or to stay awake through the night (n = 10). In the sleeping subjects Salmonella abortus equi endotoxin (0.4 ng/kg) or placebo were intravenously injected in balanced order during the first SWS episode. The age-matched, sleep-deprived subjects were injected at the same time point.
  
  
  RESULTS
  As expected, endotoxin significantly increased rectal temperature, the plasma levels of cortisol, tumor necrosis factor-alpha (TNF-alpha), the soluble TNF receptors p55 and p75, Interleukin (IL)-6, the IL-1 receptor antagonist (RA), leukocyte, and granulocyte counts in both sleeping and sleep-deprived subjects, whereas lymphocyte and monocyte counts were transiently reduced. Time courses of endotoxin-induced host responses did not differ between the sleep and sleep deprivation groups. Endotoxin did not affect the amount of nocturnal wakefulness, nonrapid-eye-movement (NREM) sleep, or rapid-eye-movement (REM) sleep across the total night compared with placebo, but significantly increased electroencephalogram-arousals (EEG-arousals) in stage 2 and decreased arousals in SWS. In addition, the amount of SWS, spectral EEG-delta and -theta power was increased at the beginning and at the end of the sleep period, respectively, when the degree of immune activation was relatively low.
  
  
  CONCLUSIONS
  The present results support the notion that short-term sleep deprivation is unlikely to harm the immune system as far as unspecific acute responses are concerned. The effects of endotoxin on sleep in this case support prior observations that in humans, enhanced SWS and intensified NREM sleep occur when host defense activation is subtle.
authors.affiliation: Max Planck Institute of Psychiatry, Munich, Germany.
authors.forename: M
authors.initials: M
authors.lastname: Haack
authors.forename: A
authors.initials: A
authors.lastname: Schuld
authors.forename: T
authors.initials: T
authors.lastname: Kraus
authors.forename: T
authors.initials: T
authors.lastname: Pollmächer
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000097:blood; D001143:Arousal / Q000502:physiology; D001427:Bacterial Toxins / Q000276:immunology*; D016207:Cytokines / Q000097:blood*; D003700:Delta Rhythm; D004731:Endotoxins / Q000276:immunology*; D006098:Granulocytes / Q000276:immunology; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6 / Q000097:blood; D007958:Leukocyte Count; D018655:Lymphocyte Count; D008297:Male; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D012016:Reference Values; D012795:Sialoglycoproteins / Q000097:blood; D016037:Single-Blind Method; D012892:Sleep Deprivation / Q000276:immunology*; D012894:Sleep Stages / Q000502:physiology*; D013826:Theta Rhythm; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D001427:Bacterial Toxins; D016207:Cytokines; D004731:Endotoxins; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; C027952:salmonella toxin; D006854:Hydrocortisone