       Document 0438
 DOCN  M9630438
 TI    Influence of host defense activation on sleep in humans.
 DT    9603
 AU    Pollmacher T; Mullington J; Korth C; Hinze-Selch D; Max-Planck-Institute
       of Psychiatry, Clinical Institute, Munich,; Germany.
 SO    Adv Neuroimmunol. 1995;5(2):155-69. Unique Identifier : AIDSLINE
       MED/96043882
 AB    Despite considerable progress in our understanding of the phenomenology
       of sleep and wakefulness, their regulation and peculiar functions are
       poorly understood. Recent animal research has revealed considerable
       evidence for interactions between host defense and sleep. Therefore, it
       has been hypothesized that host response mediators, mainly cytokines
       like interleukin-1 (IL-1), are involved in physiological sleep
       regulation. Furthermore, it has been suggested that sleep, and non rapid
       eye movement (NREM) sleep in particular, has an immuno-supportive
       function. In humans, sleep-host defense interactions are just starting
       to be understood. There is quite good evidence that some viral diseases
       cause excessive sleepiness. Other infectious diseases induce, however,
       serious disturbances of the distribution of sleep and wakefulness rather
       than excessive sleep. In addition, some disorders with excessive sleep,
       daytime fatigue or disturbed night sleep as prominent symptoms are
       thought to involve, at least in part, immuno-pathophysiological
       mechanisms. Experimental settings have only recently been used to
       elucidate host defense-sleep interactions in humans. The effects of
       endotoxin, a cell-wall lipopolysaccharide of gram-negative bacteria, on
       sleep have been tested in different settings in healthy volunteers.
       Endotoxin transiently suppresses rapid eye movement (REM) sleep
       independently of the time of the day of administration. Only low doses,
       given in the evening, promote NREM sleep. Electorencephalogram (EEG)
       power in higher frequency bands is enhanced during NREM sleep, whereas
       delta activity is not affected. In rats and rabbits, on the other hand,
       the effects of endotoxin and of the mediators of its activity on REM
       sleep are variable. Enhanced NREM sleep is a common finding and most
       pronounced during the active part of the nycthemeron and, in general,
       EEG delta activity is augmented. In view of these species differences,
       hypotheses regarding the underlying mechanisms and the biological
       significance of host defense-sleep interactions, primarily derived from
       the results of animal studies, may not entirely fit human physiology.
       They should therefore be re-evaluated and probably modified, through the
       use of additional experimental approaches in humans.
 DE    Animal  Bacterial Infections/COMPLICATIONS/PHYSIOPATHOLOGY
       Endotoxins/PHARMACOLOGY  Fatigue Syndrome, Chronic/PHYSIOPATHOLOGY
       Fibromyalgia/PHYSIOPATHOLOGY  Human  HIV
       Infections/COMPLICATIONS/PHYSIOPATHOLOGY  Immune System/PHYSIOLOGY
       Mental Disorders/PHYSIOPATHOLOGY  Narcolepsy/PHYSIOPATHOLOGY
       Neuroimmunomodulation/PHYSIOLOGY  Rabbits  Rats  Sleep/DRUG
       EFFECTS/*PHYSIOLOGY  Sleep Disorders/ETIOLOGY  Support, Non-U.S. Gov't
       Virus Diseases/COMPLICATIONS/PHYSIOPATHOLOGY  JOURNAL ARTICLE  REVIEW
       REVIEW, ACADEMIC

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

