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dc.creatorPérez, Astrides_ES
dc.creatorPoza, Margaritaes_ES
dc.creatorAranda, Jesúses_ES
dc.creatorLatasa Osta, Cristinaes_ES
dc.creatorMedrano, Francisco Javieres_ES
dc.creatorTomás, Maríaes_ES
dc.creatorRomero, Antonioes_ES
dc.creatorLasa Uzcudun, Íñigoes_ES
dc.creatorBou, Germánes_ES
dc.date.accessioned2019-01-17T08:42:15Z
dc.date.available2019-01-17T08:42:15Z
dc.date.issued2012
dc.identifier.issn0066-4804 (Print)
dc.identifier.issn1098-6596 (Electronic)
dc.identifier.urihttps://hdl.handle.net/2454/32008
dc.description.abstractControl of membrane permeability is a key step in regulating the intracellular concentration of antibiotics. Efflux pumps confer innate resistance to a wide range of toxic compounds such as antibiotics, dyes, detergents, and disinfectants in members of the Enterobacteriaceae. The AcrAB-TolC efflux pump is involved in multidrug resistance in Enterobacter cloacae. However, the underlying mechanism that regulates the system in this microorganism remains unknown. In Escherichia coli, the transcription of acrAB is upregulated under global stress conditions by proteins such as MarA, SoxS, and Rob. In the present study, two clinical isolates of E. cloacae, EcDC64 (a multidrug-resistant strain overexpressing the AcrAB-TolC efflux pump) and Jc194 (a strain with a basal AcrAB-TolC expression level), were used to determine whether similar global stress responses operate in E. cloacae and also to establish the molecular mechanisms underlying this response. A decrease in susceptibility to erythromycin, tetracycline, telithromycin, ciprofloxacin, and chloramphenicol was observed in clinical isolate Jc194 and, to a lesser extent in EcDC64, in the presence of salicylate, decanoate, tetracycline, and paraquat. Increased expression of the acrAB promoter in the presence of the above-described conditions was observed by flow cytometry and reverse transcription-PCR, by using a reporter fusion protein (green fluorescent protein). The expression level of the AcrAB promoter decreased in E. cloacae EcDC64 derivates deficient in SoxS, RobA, and RamA. Accordingly, the expression level of the AcrAB promoter was higher in E. cloacae Jc194 strains overproducing SoxS, RobA, and RamA. Overall, the data showed that SoxS, RobA, and RamA regulators were associated with the upregulation of acrAB, thus conferring antimicrobial resistance as well as a stress response in E. cloacae. In summary, the regulatory proteins SoxS, RobA, and RamA were cloned and sequenced for the first time in this species. The involvement of these proteins in conferring antimicrobial resistance through upregulation of acrAB was demonstrated in E. cloacae.en
dc.description.sponsorshipThis study was supported by Ayudas a la Movilidad (SEIMC), the Fondo de Investigaciones Sanitarias (PI081368, PS09/00687), and SERGAS (PS07/90) and a grant from the Xunta de Galicia (07CSA050916PR) to G.B. A.P. received scholarships from REIPI (Spanish Network for Research in Infectious Diseases).en
dc.format.extent11 p.
dc.format.mimetypeapplication/pdfen
dc.language.isoengen
dc.publisherAmerican Society for Microbiologyen
dc.relation.ispartofAntimicrobial Agents and Chemotherapy, December 2012 Volume 56 Number 12, p. 6256-6266en
dc.rights© 2012, American Society for Microbiology. All Rights Reserved.en
dc.subjectTranscriptional activatorsen
dc.subjectSoxSen
dc.subjectRobAen
dc.subjectRamAen
dc.subjectExpression of multidrug efflux pump AcrAB-TolCen
dc.subjectEnterobacter cloacaeen
dc.titleEffect of transcriptional activators SoxS, RobA, and RamA on expression of multidrug efflux pump AcrAB-TolC in enterobacter cloacaeen
dc.typeinfo:eu-repo/semantics/articleen
dc.typeArtículo / Artikuluaes
dc.contributor.departmentIdAB – Instituto de Agrobiotecnología / Agrobioteknologiako Institutuaes
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessen
dc.rights.accessRightsAcceso abierto / Sarbide irekiaes
dc.identifier.doi10.1128/aac.01085-12
dc.relation.publisherversionhttps://doi.org/10.1128/aac.01085-12
dc.type.versioninfo:eu-repo/semantics/publishedVersionen
dc.type.versionVersión publicada / Argitaratu den bertsioaes


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