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First published online August 8, 2008
Journal of Experimental Biology 211, 2712-2724 (2008)
Published by The Company of Biologists 2008
doi: 10.1242/jeb.014878
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Hormonal regulation of the humoral innate immune response in Drosophila melanogaster

Thomas Flatt1, Andreas Heyland2, Florentina Rus3, Ermelinda Porpiglia3, Chris Sherlock3,{dagger}, Rochele Yamamoto1, Alina Garbuzov1, Subba R. Palli4, Marc Tatar1 and Neal Silverman3,*

1 Division of Biology and Medicine, Department of Ecology and Evolutionary Biology, Brown University, Providence, RI 02912, USA
2 Department of Integrative Biology, University of Guelph, Ontario, Canada, N1G 2W1
3 Department of Medicine, Division of Infectious Disease, University of Massachusetts Medical School, Worcester, MA 01655, USA
4 Department of Entomology, Agricultural Science Center, College of Agriculture, University of Kentucky, Lexington, KY 40546-0091, USA

* Corresponding author (e-mail: neal.silverman{at}umassmed.edu)

Accepted 3 June 2008

Juvenile hormone (JH) and 20-hydroxy-ecdysone (20E) are highly versatile hormones, coordinating development, growth, reproduction and aging in insects. Pulses of 20E provide key signals for initiating developmental and physiological transitions, while JH promotes or inhibits these signals in a stage-specific manner. Previous evidence suggests that JH and 20E might modulate innate immunity, but whether and how these hormones interact to regulate the immune response remains unclear. Here we show that JH and 20E have antagonistic effects on the induction of antimicrobial peptide (AMP) genes in Drosophila melanogaster. 20E pretreatment of Schneider S2* cells promoted the robust induction of AMP genes, following immune stimulation. On the other hand, JH III, and its synthetic analogs (JHa) methoprene and pyriproxyfen, strongly interfered with this 20E-dependent immune potentiation, although these hormones did not inhibit other 20E-induced cellular changes. Similarly, in vivo analyses in adult flies confirmed that JH is a hormonal immuno-suppressor. RNA silencing of either partner of the ecdysone receptor heterodimer (EcR or Usp) in S2* cells prevented the 20E-induced immune potentiation. In contrast, silencing methoprene-tolerant (Met), a candidate JH receptor, did not impair immuno-suppression by JH III and JHa, indicating that in this context MET is not a necessary JH receptor. Our results suggest that 20E and JH play major roles in the regulation of gene expression in response to immune challenge.

Key words: Drosophila, innate immunity, humoral immune response, antimicrobial peptides, juvenile hormone, ecdysone, hormone receptors


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[Abstract] [Full Text] [PDF]




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