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dc.contributor.authorApidianakis, Yiorgosen
dc.contributor.authorMindrinos, M. N.en
dc.contributor.authorXiao, W.en
dc.contributor.authorLau, G. W.en
dc.contributor.authorBaldini, R. L.en
dc.contributor.authorDavis, R. W.en
dc.contributor.authorRahme, L. G.en
dc.date.accessioned2019-11-04T12:50:13Z
dc.date.available2019-11-04T12:50:13Z
dc.date.issued2005
dc.identifier.urihttp://gnosis.library.ucy.ac.cy/handle/7/52934
dc.description.abstractInsights into the host factors and mechanisms mediating the primary host responses after pathogen presentation remain limited, due in part to the complexity and genetic intractability of host systems. Here, we employ the model Drosophila melanogaster to dissect and identify early host responses that function in the initiation and progression of Pseudomonas aeruginosa pathogenesis. First, we use immune potentiation and genetic studies to demonstrate that flies mount a heightened defense against the highly virulent P. aeruginosa strain PA14 when first inoculated with strain CF5, which is avirulent in fliesen
dc.description.abstractthis effect is mediated via the Imd and Toll signaling pathways. Second, we use whole-genome expression profiling to assess and compare the Drosophila early defense responses triggered by the PA14 vs. CF5 strains to identify genes whose expression patterns are different in susceptible vs. resistant host-pathogen interactions, respectively. Our results identify pathogenesis- and defense-specific genes and uncover a previously undescribed mechanism used by P. aeruginosa in the initial stages of its host interaction: suppression of Drosophila defense responses by limiting antimicrobial peptide gene expression. These results provide insights into the genetic factors that mediate or restrict pathogenesis during the early stages of the bacterial-host interaction to advance our understanding of P. aeruginosa-human infections.en
dc.sourceProceedings of the National Academy of Sciences of the United States of Americaen
dc.source.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-14044277610&doi=10.1073%2fpnas.0409588102&partnerID=40&md5=533e07bd011475c753732835181bebe0
dc.subjectarticleen
dc.subjectHumansen
dc.subjectpriority journalen
dc.subjectgene expression regulationen
dc.subjectnonhumanen
dc.subjectimmune responseen
dc.subjectAnimalsen
dc.subjectSignal Transductionen
dc.subjectantiinfective agenten
dc.subjectbacterial strainen
dc.subjectPseudomonas aeruginosaen
dc.subjectPseudomonas Infectionsen
dc.subjectnucleotide sequenceen
dc.subjectGene Expression Profilingen
dc.subjectgene identificationen
dc.subjectBacteria (microorganisms)en
dc.subjectbacterial virulenceen
dc.subjectDrosophila melanogasteren
dc.subjectVirulenceen
dc.subjectDrosophila Proteinsen
dc.subjectAntimicrobial Cationic Peptidesen
dc.subjecthost resistanceen
dc.subjectImmune potentiationen
dc.subjectImmunity, Naturalen
dc.subjectInnate immunityen
dc.subjectMelanogasteren
dc.subjectNegibacteriaen
dc.subjectPathogenesisen
dc.subjectPseudomonasen
dc.subjectReceptors, Cell Surfaceen
dc.subjectSuppression, Geneticen
dc.subjectToll-Like Receptorsen
dc.titleProfiling early infection responses: Pseudomonas aeruginosa eludes host defenses by suppressing antimocrobial peptide gene expressionen
dc.typeinfo:eu-repo/semantics/article
dc.identifier.doi10.1073/pnas.0409588102
dc.description.volume102
dc.description.startingpage2573
dc.description.endingpage2578
dc.type.uhtypeArticleen
dc.description.notes<p>Cited By :107</p>en
dc.source.abbreviationProc.Natl.Acad.Sci.U.S.A.en
dc.contributor.orcidApidianakis, Yiorgos [0000-0002-7465-3560]


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