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Steroid Hormone Signaling Is Essential to Regulate Innate Immune Cells and Fight Bacterial Infection in Drosophila

dc.contributor.authorRegan, Jennifer C.
dc.contributor.authorBrandão, Ana S.
dc.contributor.authorLeitão, Alexandre B.
dc.contributor.authorMantas Dias, Ângela Raquel
dc.contributor.authorSucena, Élio
dc.contributor.authorJacinto, António
dc.contributor.authorZaidman-Rémy, Anna
dc.date.accessioned2015-11-09T12:41:15Z
dc.date.available2015-11-09T12:41:15Z
dc.date.issued2013-10-24
dc.description.abstractCoupling immunity and development is essential to ensure survival despite changing internal conditions in the organism. Drosophila metamorphosis represents a striking example of drastic and systemic physiological changes that need to be integrated with the innate immune system. However, nothing is known about the mechanisms that coordinate development and immune cell activity in the transition from larva to adult. Here, we reveal that regulation of macrophage-like cells (hemocytes) by the steroid hormone ecdysone is essential for an effective innate immune response over metamorphosis. Although it is generally accepted that steroid hormones impact immunity in mammals, their action on monocytes (e.g. macrophages and neutrophils) is still not well understood. Here in a simpler model system, we used an approach that allows in vivo, cell autonomous analysis of hormonal regulation of innate immune cells, by combining genetic manipulation with flow cytometry, high-resolution time-lapse imaging and tissue-specific transcriptomic analysis. We show that in response to ecdysone, hemocytes rapidly upregulate actin dynamics, motility and phagocytosis of apoptotic corpses, and acquire the ability to chemotax to damaged epithelia. Most importantly, individuals lacking ecdysone-activated hemocytes are defective in bacterial phagocytosis and are fatally susceptible to infection by bacteria ingested at larval stages, despite the normal systemic and local production of antimicrobial peptides. This decrease in survival is comparable to the one observed in pupae lacking immune cells altogether, indicating that ecdysone-regulation is essential for hemocyte immune functions and survival after infection. Microarray analysis of hemocytes revealed a large set of genes regulated at metamorphosis by EcR signaling, among which many are known to function in cell motility, cell shape or phagocytosis. This study demonstrates an important role for steroid hormone regulation of immunity in vivo in Drosophila, and paves the way for genetic dissection of the mechanisms at work behind steroid regulation of innate immune cells.pt_PT
dc.description.sponsorshipFCT fellowships: (SFRH/BPD/44613/2008, SFRH/BD/51175/2010), EMBO: (ALTF 178-2009), Gulbenkian Institute PhD Program.pt_PT
dc.identifier10.1371/journal.ppat.1003720
dc.identifier.citationRegan JC, Branda˜o AS, Leita˜o AB, Mantas Dias Aˆ R, Sucena E´ , et al. (2013) Steroid Hormone Signaling Is Essential to Regulate Innate Immune Cells and Fight Bacterial Infection in Drosophila. PLoS Pathog 9(10): e1003720. doi:10.1371/journal.ppat.1003720pt_PT
dc.identifier.doi10.1371/journal.ppat.1003720
dc.identifier.urihttp://hdl.handle.net/10400.7/477
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherPLOSpt_PT
dc.relationEpithelial Resealing
dc.relation.publisherversionhttp://www.plospathogens.org/article/Authors/info:doi/10.1371/journal.ppat.1003720pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectDrosophila melanogasterpt_PT
dc.subjectGene expressionpt_PT
dc.subjectGene regulationpt_PT
dc.subjectHemocytespt_PT
dc.subjectLarvaept_PT
dc.subjectMetamorphosispt_PT
dc.subjectMetamorphosispt_PT
dc.subjectPhagocytosispt_PT
dc.subjectPupaept_PT
dc.titleSteroid Hormone Signaling Is Essential to Regulate Innate Immune Cells and Fight Bacterial Infection in Drosophilapt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleEpithelial Resealing
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PTDC%2FBIA-BCM%2F65872%2F2006/PT
oaire.awardURIinfo:eu-repo/grantAgreement/EC/FP7/208631/EU
oaire.citation.endPage15pt_PT
oaire.citation.issue10pt_PT
oaire.citation.startPage1pt_PT
oaire.citation.titlePlos Pathogenspt_PT
oaire.citation.volume9pt_PT
oaire.fundingStream3599-PPCDT
oaire.fundingStreamFP7
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100008530
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameEuropean Commission
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isProjectOfPublication9a0e1bb9-1d1b-46ff-8765-ad0b55d2037b
relation.isProjectOfPublication22d81724-8d1f-415e-a98a-7109b2670bfd
relation.isProjectOfPublication.latestForDiscovery9a0e1bb9-1d1b-46ff-8765-ad0b55d2037b

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