CpxR activates MexAB-OprM efflux pump expression and enhances antibiotic resistance in both laboratory and clinical nalB-type isolates of Pseudomonas aeruginosa

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dc.contributor.author Tian, Zhe-Xian
dc.contributor.author Yi, Xue-Xian
dc.contributor.author Cho, Anna
dc.contributor.author O'Gara, Fergal
dc.contributor.author Wang, Yi-Ping
dc.date.accessioned 2016-10-26T09:01:12Z
dc.date.available 2016-10-26T09:01:12Z
dc.date.issued 2016-10-13
dc.identifier.citation Tian, Z.-X., Yi, X.-X., Cho, A., O’Gara, F. and Wang, Y.-P. (2016) 'CpxR activates MexAB-OprM efflux pump expression and enhances antibiotic resistance in both laboratory and clinical nalB-type isolates of Pseudomonas aeruginosa', PLoS Pathogens, 12(10), e1005932 (22pp). doi:10.1371/journal.ppat.1005932 en
dc.identifier.volume 12 en
dc.identifier.issued 10 en
dc.identifier.startpage 1 en
dc.identifier.endpage 22 en
dc.identifier.issn 1553-7366
dc.identifier.uri http://hdl.handle.net/10468/3214
dc.identifier.doi 10.1371/journal.ppat.1005932
dc.description.abstract Resistance-Nodulation-Division (RND) efflux pumps are responsible for multidrug resistance in Pseudomonas aeruginosa. In this study, we demonstrate that CpxR, previously identified as a regulator of the cell envelope stress response in Escherichia coli, is directly involved in activation of expression of RND efflux pump MexAB-OprM in P. aeruginosa. A conserved CpxR binding site was identified upstream of the mexA promoter in all genome-sequenced P. aeruginosa strains. CpxR is required to enhance mexAB-oprM expression and drug resistance, in the absence of repressor MexR, in P. aeruginosa strains PA14. As defective mexR is a genetic trait associated with the clinical emergence of nalB-type multidrug resistance in P. aeruginosa during antibiotic treatment, we investigated the involvement of CpxR in regulating multidrug resistance among resistant isolates generated in the laboratory via antibiotic treatment and collected in clinical settings. CpxR is required to activate expression of mexAB-oprM and enhances drug resistance, in the absence or presence of MexR, in ofloxacin-cefsulodin-resistant isolates generated in the laboratory. Furthermore, CpxR was also important in the mexR-defective clinical isolates. The newly identified regulatory linkage between CpxR and the MexAB-OprM efflux pump highlights the presence of a complex regulatory network modulating multidrug resistance in P. aeruginosa. en
dc.description.sponsorship National Science Foundation of China (Grant Nos. 31270127 and 81071398); State Key Laboratory of Protein and Plant Gene Research, China (Grant B02); National Science Fund for Distinguished Young Scholars, China (Grant No. 39925017) en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Public Library of Science en
dc.rights © 2016, Tian et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. en
dc.rights.uri https://creativecommons.org/licenses/by/4.0/ en
dc.subject Multidrug resistance en
dc.subject Antibiotic en
dc.subject Regulatory en
dc.title CpxR activates MexAB-OprM efflux pump expression and enhances antibiotic resistance in both laboratory and clinical nalB-type isolates of Pseudomonas aeruginosa en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother Fergal O'Gara, Microbiology, University College Cork, Cork, Ireland. +353-21-490-3000 Email: f.ogara@ucc.ie en
dc.internal.availability Full text available en
dc.description.version Published Version en
dc.contributor.funder National Natural Science Foundation of China en
dc.contributor.funder State Key Laboratory of Protein and Plant Gene Research, China
dc.contributor.funder National Science Fund for Distinguished Young Scholars, China
dc.description.status Peer reviewed en
dc.identifier.journaltitle PLoS Pathogens en
dc.internal.IRISemailaddress f.ogara@ucc.ie
dc.identifier.articleid e1005932


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© 2016, Tian et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Except where otherwise noted, this item's license is described as © 2016, Tian et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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