Psychother Psychosom Med Psychol 2005; 55(1): 29-35
DOI: 10.1055/s-2004-834561
Originalarbeit
© Georg Thieme Verlag KG Stuttgart · New York

Experimentelle Untersuchungen der Interaktion zwischen Schlaf und Immunsystem beim Menschen

Experimental Studies on the Interaction Between Sleep and the Immune System in HumansAndreas  Schuld1 , Monika  Haack2 , Dunja  Hinze-Selch3 , Janet  Mullington2 , Thomas  Pollmächer1
  • 1Max-Planck-Institut für Psychiatrie, München, Deutschland
  • 2Department of Neurology, Beth Israel Deaconess Medical Center & Harvard Medical School, Boston, MA, USA
  • 3Klinik für Psychiatrie und Psychotherapie, Universitätsklinikum Schleswig-Holstein, Campus Kiel
Unterstützt durch die Volkswagenstiftung, Hannover (I/71979)
Further Information

Publication History

Eingegangen: 28. Oktober 2003

Angenommen: 2. November 2004

Publication Date:
13 January 2005 (online)

Zusammenfassung

Müdigkeit und vermehrtes Schlafbedürfnis sind typische Symptome entzündlicher und infektiöser Erkrankungen. Die Annahme ist weit verbreitet, der Schlaf habe eine immunsupportive Funktion. Die vorliegende Arbeit fasst die Datenlage hinsichtlich der experimentellen Erforschung der Interaktion zwischen Schlaf und Immunsystem beim Menschen zusammen. Das Schlaf-wach-Verhalten reagiert auf eine experimentelle Aktivierung immunologischer Prozesse (z. B. durch die Gabe von bakteriellem Endotoxin) sehr sensibel. Neben der durch Endotoxingabe ausgelösten Fieberreaktion und neuroendokrinen Aktivierung kommt es oft auch zu einer Störung der Nachtschlafkontinuität. Wenn hingegen durch geringere Mengen Endotoxin die Freisetzung inflammatorischer Zytokine stimuliert, aber weder die Körpertemperatur noch neuroendokrine Systeme beeinflusst werden, so kommt es zu einer Zunahme des Non-REM-Schlafes. Dies erklärt sich wahrscheinlich durch Veränderungen in der biologischen Aktivität des Tumor-Nekrose-Faktor-α(TNF-α)-Systems. Neben ihrer Funktion im Verlaufe der Wirtsantwort scheinen Zytokine aber auch in der physiologischen Schlaf-wach-Regulation eine zentrale Rolle zu spielen, obschon die Datenlage hierzu noch nicht ausreichend ist. Unklar ist bis heute, ob der Schlaf tatsächlich körpereigene Abwehrprozesse unterstützt: Akuter Schlafentzug von bis zu 55 Stunden hat zwar keinen nennenswerten Einfluss auf die endotoxininduzierte primäre Wirtsantwort, allerdings gibt es einige, wenn auch bisher nicht konsistente Hinweise darauf, dass Schlafentzug möglicherweise Aspekte spezifischer Immunität, wie etwa die Bildung von Antikörpern gegen virale Antigene, negativ beeinflusst.

Abstract

Sleepiness and increased sleep pressure are typical symptoms of inflammation and infection. Moreover, it is a pre-scientific belief that sleep supports host defense. The present paper summarizes the experimental evidence regarding the interaction between sleep and the immune system in humans. Sleep-wake behavior is very sensitive to experimental host defense activation, for example, by bacterial endotoxin. When the injection of endotoxin is accompanied by fever and a prominent neuroendocrine activation, sleep continuity will be disturbed. When the production of inflammatory cytokines is stimulated by smaller amounts of endotoxin, but no fever and no neuroendocrine activation are apparent, the nonREM-sleep amount will increase. This is possibly due to changes in the biological activity of the tumor necrosis factor-α (TNF-α) system. Besides their important function in sleep regulation during acute immune response, cytokines also seem to be involved in physiological sleep regulation, although there still is not very much data on this issue. So far, it remains largely unknown whether or not sleep supports host defense. In humans, for example, acute sleep deprivation up to 55 hours has only minor effects on endotoxin-induced host responses. In contrast, there is preliminary and yet inconsistent evidence that sleep deprivation might impair antibody formation in response to viral challenges.

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Prof. Dr. Thomas Pollmächer

Zentrum für psychische Gesundheit · Klinikum Ingolstadt

Postfach 210662

85021 Ingoldstadt

Email: thomas.pollmaecher@klinikum-ingolstadt.de

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