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dc.contributor.authorMachuca, Jesúses_ES
dc.contributor.authorRecacha, Estheres_ES
dc.contributor.authorBriales, Alejandraes_ES
dc.contributor.authorDíaz-de-Alba, Paulaes_ES
dc.contributor.authorBlázquez Gómez, Jesúses_ES
dc.contributor.authorPascual, Álvaroes_ES
dc.contributor.authorRodríguez-Martínez, José-Manueles_ES
dc.date.accessioned2019-04-26T12:17:41Z-
dc.date.available2019-04-26T12:17:41Z-
dc.date.issued2017-07-19-
dc.identifier.citationFrontiers in Microbiology 8: 1370 (2017)es_ES
dc.identifier.urihttp://hdl.handle.net/10261/180645-
dc.description.abstractBactericidal activity of quinolones has been related to a combination of DNA fragmentation, reactive oxygen species (ROS) production and programmed cell death (PCD) systems. The underlying molecular systems responsible for reducing bactericidal effect during antimicrobial therapy in low-level quinolone resistance (LLQR) phenotypes need to be clarified. To do this and also define possible new antimicrobial targets, the transcriptome profile of isogenic Escherichia coli harboring quinolone resistance mechanisms in the presence of a clinical relevant concentration of ciprofloxacin was evaluated. A marked differential response to ciprofloxacin of either up- or downregulation was observed in LLQR strains. Multiple genes implicated in ROS modulation (related to the TCA cycle, aerobic respiration and detoxification systems) were upregulated (sdhC up to 63.5-fold) in mutants with LLQR. SOS system components were downregulated (recA up to 30.7-fold). yihE, a protective kinase coding for PCD, was also upregulated (up to 5.2-fold). SdhC inhibition sensitized LLQR phenotypes (up to ΔLog = 2.3 after 24 h). At clinically relevant concentrations of ciprofloxacin, gene expression patterns in critical systems to bacterial survival and mutant development were significantly modified in LLQR phenotypes. Chemical inhibition of SdhC (succinate dehydrogenase) validated modulation of ROS as an interesting target for bacterial sensitization.es_ES
dc.description.sponsorshipThis work was supported by the Ministerio de Sanidad y Consumo, Instituto de Salud Carlos III (projects PI11-00934 and PI14/00940) and the Consejería de Innovación, Ciencia y Empresa, Junta de Andalucía (P11-CTS-7730), Spain, by the Plan Nacional de I+D+i 2008–2011 and the Instituto de Salud Carlos III, Subdirección General de Redes y Centros de Investigación Cooperativa, Ministerio de Economía y Competitividad, the Spanish Network for Research in Infectious Diseases (REIPI RD12/0015)—co-financed by European Development Regional Fund ‘A way to achieve Europe’ ERDF.es_ES
dc.language.isoenges_ES
dc.publisherFrontiers Mediaes_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rightsopenAccesses_ES
dc.subjectCiprofloxacines_ES
dc.subjectLow-level quinolone resistancees_ES
dc.subjectSurvivales_ES
dc.subjectTranscriptomices_ES
dc.subjectGlobal responsees_ES
dc.subjectSensitizationes_ES
dc.titleCellular Response to Ciprofloxacin in Low-Level Quinolone-Resistant Escherichia colies_ES
dc.typeartículoes_ES
dc.identifier.doi10.3389/fmicb.2017.01370-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.3389/fmicb.2017.01370es_ES
dc.identifier.e-issn1664-302X-
dc.rights.licensehttp://creativecommons.org/licenses/by/4.0/es_ES
dc.contributor.funderMinisterio de Sanidad y Consumo (España)es_ES
dc.contributor.funderInstituto de Salud Carlos IIIes_ES
dc.contributor.funderJunta de Andalucíaes_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.contributor.funderEuropean Commissiones_ES
dc.relation.csices_ES
oprm.item.hasRevisionno ko 0 false*
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000780es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
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