Acute sleep deprivation enhances post-infection sleep and promotes survival during bacterial infection in Drosophila.
OBJECTIVE
Sleep is known to increase as an acute response to infection. However, the function of this behavioral response in host defense is not well understood. To address this problem, we evaluated the effect of acute sleep deprivation on post-infection sleep and immune function in Drosophila.


METHODS
Laboratory.


METHODS
Drosophila melanogaster.


RESULTS
Flies were subjected to sleep deprivation before (early DEP) or after (late DEP) bacterial infection. Relative to a non-deprived control, flies subjected to early DEP had enhanced sleep after infection as well as increased bacterial clearance and survival outcome. Flies subjected to late DEP experienced enhanced sleep following the deprivation period, and showed a modest improvement in survival outcome. Continuous DEP (early and late DEP) throughout infection also enhanced sleep later during infection and improved survival. However, improved survival in flies subjected to late or continuous DEP did not occur until after flies had experienced sleep. During infection, both early and late DEP enhanced NFκB transcriptional activity as measured by a luciferase reporter (κB-luc) in living flies. Early DEP also increased NFκB activity prior to infection. Flies that were deficient in expression of either the Relish or Dif NFκB transcription factors showed normal responses to early DEP. However, the effect of early DEP on post-infection sleep and survival was abolished in double mutants, which indicates that Relish and Dif have redundant roles in this process.


CONCLUSIONS
Acute sleep deprivation elevated NFκB-dependent activity, increased post-infection sleep, and improved survival during bacterial infection.
Center for Sleep and Circadian Neurobiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA.
Tzu-Hsing
TH
Kuo
Center for Sleep and Circadian Neurobiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA.
Julie A
JA
Williams
D000818:Animals; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism; D004331:Drosophila melanogaster / Q000235:genetics / Q000276:immunology / Q000382:microbiology* / Q000502:physiology*; D005260:Female; D016328:NF-kappa B / Q000378:metabolism; D012890:Sleep / Q000235:genetics / Q000276:immunology* / Q000502:physiology*; D012892:Sleep Deprivation / Q000276:immunology* / Q000503:physiopathology*; D016019:Survival Analysis; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism
D004268:DNA-Binding Proteins; C084428:Dif protein, Drosophila; D029721:Drosophila Proteins; D016328:NF-kappa B; C101626:Rel protein, Drosophila; D014157:Transcription Factors
Drosophila; NFkappaB; bacterial infection; immune response; sleep deprivation