• Open Access

Aging of the innate immune response in Drosophila melanogaster

Authors

  • Melissa Zerofsky,

    1. Brown University, Division of Biology and Medicine, Providence, RI, USA
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    • *

      MZ and EH contributed equally to this paper.

  • Ephat Harel,

    1. Brown University, Division of Biology and Medicine, Providence, RI, USA
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    • *

      MZ and EH contributed equally to this paper.

  • Neal Silverman,

    1. University of Massachusetts Medical School, Department of Medicine, Division of Infectious Disease, Worchester, MA, USA
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  • Marc Tatar

    Corresponding author
    1. Brown University, Division of Biology and Medicine, Providence, RI, USA

      Marc Tatar, Box GW, Division of Biology and Medicine, Brown University, Providence, RI 02912, USA. Tel.: +1 401 863 3455; fax: +1 401 863 2166; e-mail: Marc_Tatar@Brown.edu
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Marc Tatar, Box GW, Division of Biology and Medicine, Brown University, Providence, RI 02912, USA. Tel.: +1 401 863 3455; fax: +1 401 863 2166; e-mail: Marc_Tatar@Brown.edu

Summary

Increased activation of the innate immune system is a common feature of aging animals, including mammals and Drosophila melanogaster. With age, D. melanogaster progressively express higher levels of many antimicrobial peptides. It is unknown, however, whether this pattern reflects age-dependent changes in the function of the immune system itself or arises simply because aged adults have greater cumulative exposure to pathogens. Here we demonstrate that aged D. melanogaster transcribe more antimicrobial diptericin when experimentally exposed to septic bacterial infections. This strong net response in older females is the result of persistent diptericin transcription upon septic exposure, whereas young females rapidly terminate this induction. In contrast to their response to septic exposure, when exposed to killed bacteria aged females have less capacity to induce diptericin. Because this functional capacity of innate immunity declines with age, we conclude that female Drosophila undergo immune senescence. Furthermore, we show that fecundity is reduced by induction of innate immunity via the immune deficiency pathway. Consequently, maximum reproduction will occur when the immune response is tightly controlled in young females, even if this increases infection risk at later ages.

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