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<dc:title xml:lang="en">Drosophila responses upon exposure to a phenylpyrazole pesticide, fipronil and/or after the infection by an intracellular parasite, the microsporidium Tubulinosema ratisbonensis</dc:title>
<dcterms:alternative xml:lang="fr">Réponses de la drosophile à l’exposition à un pesticide, le fipronil et à une infection par un parasite intracellulaire, la microsporidie Tubulinosema ratisbonensis</dcterms:alternative>
<dc:subject xml:lang="fr">Microsporidie</dc:subject>
<dc:subject xml:lang="fr">Fipronil</dc:subject>
<dc:subject xml:lang="fr">Drosophile</dc:subject>
<dc:subject xml:lang="fr">Lipides</dc:subject>
<dc:subject xml:lang="fr">Immunité</dc:subject>
<dc:subject xml:lang="fr">Phagocytose</dc:subject>
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<dcterms:abstract xml:lang="fr">Le déclin des abeilles est le syndrome d’effondrement de leurs colonies, est inquiétant. Les pesticides et la susceptibilité des abeilles à certaines infections contribuent à cette perte. Il est crucial de comprendre les mécanismes d’action des pesticides et parasites responsables de cette mortalité. J’ai étudié les effets de l’infection par la microsporidie T. ratisbonensis et/ou de l’insecticide fipronil chez la drosophile. Les microsporidies prolifèrent en subtilisant les lipides de l’hôte. La phagocytose est la seule réponse de l’hôte conférant une protection contre le parasite. Le fipronil induit un mécanisme de pertes lipidiques lequel repose sur la lipophagie et génère du tréhalose qui alimente un état d’hyperactivité. Le fipronil induit une production d’Akh mobilisant les réserves lipidiques et stimulant un réseau neuronal d’hyperactivité normalement induit en cas de jeûne. Ce mécanisme contribue à la sensibilité des drosophiles exposées à des doses faibles du pesticide.</dcterms:abstract>
<dcterms:abstract xml:lang="en">The decline of honeybees, colony collapse disorder, is alarming. Pesticides and the susceptibility of honeybees to some infections contribute to this loss. Understanding the mechanisms of action of pesticides and parasites responsible for this lethality is crucial. I have studied the effects of the infection by the microsporidium T. ratisbonensis and/or the fipronil insecticide in Drosophila. Microsporidia proliferate by hijacking host lipid reserves. Phagocytosis is the sole host defense conferring some protection against the parasite. Also, we have discovered a mechanism of lipidic loss upon ingestion of fipronil, which is mediated by lipophagy and produces trehalose that sustains a hyperactivity state. Fipronil indirectly induces the production of Akh, which partially mediates the mobilization of lipidic reserves and stimulates a hyperactivity neural network normally triggered by starvation. This mechanism contributes to the susceptibility of flies exposed to low doses of fipronil.</dcterms:abstract>
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