Project Schlaf und Malaria

Basic data

Schlaf und Malaria
01/07/2020 to 30/06/2023
Abstract / short description:
Infection with malaria parasites elicits sickness behavior with fatigue
as a major symptom. Tumor necrosis factor (TNF) and interleukin-1
(IL-1) are potential mediators of this neurobehavioral response. As
both cytokines are also sleep regulatory substances, an increase in
slow wave sleep (SWS) duration and intensity during the symptomatic
stage of malaria is very likely. Due to its immunosupportive properties,
SWS in turn could boost host defense mechanisms and the formation
of immunological memory against the pathogen. Analyses of sleep in
malaria are at present completely lacking. We will therefore assess
sleep changes (i) in patients with naturally acquired malaria in
Lambaréné, Africa and (ii) in malaria-naive volunteers receiving
controlled human malaria infection (CHMI) in Tübingen and will
delineate whether these sleep changes can predict the clinical course
of the infection and anti-malarial immunity, respectively. We
hypothesize that malaria infected patients and participants with most
pronounced increases in SWS duration and intensity have a
shortened time until clearance of parasitemia and clinical symptoms
and that participants with a boost in SWS after CHMI show more
robust increases in malaria-specific effector T cells and antibodies.
CHMI is a safe, highly standardized, ethically justifiable, and thus
compelling experimental infection model in humans, that will also
allow to identify potential mediators of sickness behavior and SWS
changes, like e.g., TNF, prostaglandins or adenosine. In anti-malarial
vaccination trials in Tübingen, we will moreover assess (iii) whether
habitual good sleep benefits immunological memory formation. We
expect that participants with habitual good SWS show higher malariaspecific
T cells and antibodies in the effector and memory phase and
higher protection rates upon subsequent CHMI. In an explorative
manner we will additionally decipher whether sleep prepares the
innate immune system for pathogen encounter the next day and
whether this translates into more robust adaptive immunity. In sum,
we aim to prove for the first time in humans that SWS is a host
defense mechanism that is triggered by immune activation during an
infection and in turn serves to optimize adaptive immunity against the
pathogen. Apart from gaining knowledge into basic questions of
sleep-immune research (Do infections trigger SWS in humans? What
are the mediators? Does SWS benefit innate and adaptive immunity
and immunological memory formation?) our findings will help to
optimize diagnostic tools, vaccines and treatment in malaria.
Malaria; Schlaf; Psychoneuroimmunologie

Involved staff


Institute of Medical Psychology
Non-clinical institutes, Faculty of Medicine

Local organizational units

Institute of Medical Psychology
Non-clinical institutes
Faculty of Medicine


Bonn, Nordrhein-Westfalen, Germany

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