Objective: To examine whether increased sleep during viral or bacterial inf
ections 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 sl
eeping subjects Salmonella abortus equi endotoxin (0.4 ng/kg) or placebo we
re intravenously injected in balanced order during the first SWS episode. T
he age-matched, sleep-deprived subjects were injected at the same time poin
t. Results: As expected, endotoxin significantly increased rectal temperatu
re, the plasma levels of cortisol, tumor necrosis factor-alpha (TNF-alpha),
the soluble TNF receptors p55 and p75, Interleukin (IL)-6, the IL-1 recept
or antagonist (RA), leukocyte, and granulocyte counts in both sleeping and
sleep-deprived subjects, whereas lymphocyte and monocyte counts were transi
ently reduced. Time courses of endotoxin-induced host responses did not dif
fer between the sleep and sleep deprivation groups. Endotoxin did not affec
t the amount of nocturnal wakefulness, nonrapid-eve-movement (NREM) sleep,
or rapid-eye-movement (REM) sleep across the total night compared with plac
ebo, but significantly increased electroencephalogram-arousals (EEG-arousal
s) 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 activ
ation was relatively low. Conclusion: The present results support the notio
n that short-term sleep deprivation is unlikely to harm the immune system a
s 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
.