Dissecting the mechanisms of linezolid resistance in a drosophila melanogaster infection model of staphylococcus aureus

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dc.contributor.authorDiaz, Lorena
dc.contributor.authorKontoyiannis, Dimitrios P.
dc.contributor.authorPanesso, Diana
dc.contributor.authorAlbert, Nathaniel D.
dc.contributor.authorSingh, Kavindra V.
dc.contributor.authorTran, Truc T.
dc.contributor.authorMunita, Jose M.
dc.contributor.authorMurray, Barbara E.
dc.contributor.authorArias, Cesar A.
dc.contributor.orcidPanesso, Diana [0000-0002-4049-9702]
dc.date.accessioned2020-09-14T22:08:06Z
dc.date.available2020-09-14T22:08:06Z
dc.date.issued2013
dc.description.abstractenglishBackground. Mini-host models are simple experimental systems to study host-pathogen interactions. We adapted a Drosophila melanogaster infection model to evaluate the in vivo effect of different mechanisms of linezolid (LNZ) resistance in Staphylococcus aureus. Methods. Fly survival was evaluated after infection with LNZ-resistant S. aureus strains NRS119 (which has mutations in 23S ribosomal RNA [rRNA]), CM-05 and 004-737X (which carry cfr), LNZ-susceptible derivatives of CM-05 and 004-737X (which lack cfr), and ATCC 29213 (an LNZ-susceptible control). Flies were then fed food mixed with LNZ (concentration, 15–500 µg/mL). Results were compared to those in mouse peritonitis, using LNZ via oral gavage at 80 and 120 mg/kg every 12 hours. Results. LNZ at 500 µg/mL in fly food protected against all strains, while concentrations of 15–250 µg/mL failed to protect against NRS119 (survival, 1.6%–20%). An in vivo effect of cfr was only detected at concentrations of 30 and 15 µg/mL. In the mouse peritonitis model, LNZ (at doses that mimic human pharmacokinetics) protected mice from challenge with the cfr+ 004-737X strain but was ineffective against the NRS119 strain, which carried 23S rRNA mutations. Conclusions. The fly model offers promising advantages to dissect the in vivo effect of LNZ resistance in S. aureus, and findings from this model appear to be concordant with those from the mouse peritonitis modeleng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.1093/infdis/jit138
dc.identifier.instnameinstname:Universidad El Bosquespa
dc.identifier.issn1537-6613
dc.identifier.reponamereponame:Repositorio Institucional Universidad El Bosquespa
dc.identifier.repourlhttps://repositorio.unbosque.edu.co
dc.identifier.urihttps://hdl.handle.net/20.500.12495/4085
dc.language.isoeng
dc.publisherOxford University Pressspa
dc.publisher.journalJournal of Infectious Diseasesspa
dc.relation.ispartofseriesJournal of Infectious Diseases, 1537-6613, Vol 208, Nro 1, 2013, pag 83-91spa
dc.relation.urihttps://academic.oup.com/jid/article/208/1/83/796362
dc.rights.accessrightshttps://purl.org/coar/access_right/c_abf2
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess
dc.rights.accessrightsAcceso abierto
dc.rights.creativecommons2013-07-01
dc.rights.localAcceso abiertospa
dc.subject.decsBacilos grampositivos formadores de endosporasspa
dc.subject.decsAcetamidasspa
dc.subject.decsFarmacorresistencia bacterianaspa
dc.subject.keywordsStaphylococcus aureusspa
dc.subject.keywordsLinezolidspa
dc.subject.keywordsResistancespa
dc.subject.keywordsDrosophila melanogasterspa
dc.titleDissecting the mechanisms of linezolid resistance in a drosophila melanogaster infection model of staphylococcus aureusspa
dc.title.translatedDissecting the mechanisms of linezolid resistance in a drosophila melanogaster infection model of staphylococcus aureusspa
dc.type.coarhttps://purl.org/coar/resource_type/c_6501
dc.type.driverinfo:eu-repo/semantics/article
dc.type.hasversioninfo:eu-repo/semantics/publishedVersion
dc.type.localArtículo de revista

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