Journal
FRONTIERS IN MICROBIOLOGY
Volume 6, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fmicb.2015.00008
Keywords
Pseudomonas aeruginosa; efflux; mexXY-oprA; mexEF-oprN; mexS
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Funding
- Japan Society for the Promotion of Science [23790106, 26460080]
- Institute of Pharmaceutical Life Sciences, Aichi Gakuin University
- Grants-in-Aid for Scientific Research [23790106, 26460080] Funding Source: KAKEN
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The emergence of multidrug-resistant Pseudomonas aeruginosa has become a serious problem in medical settings. P aeruginosa clinical isolate PA7 is resistant to fluoroquinolones, aminoglycosides, and most Hactams but not imipenem. In this study, enhanced efflux-mediated fluoroquinolone resistance of PA7 was shown to reflect increased expression of two resistance nodulation cell division (RND) -type multidrug efflux operons, mexEF-oprN and mexXY-oprA. Such a clinical isolate has rarely been reported because MexEF-OprN-overproducing mutants often increase susceptibility to aminoglycosides apparently owing to impairment of the MexXY system. A mutant of PA7 lacking three RND-type multidrug efflux operons (mexAB-oprM, mexEF-oprN, and mexXY-oprA) was susceptible to all anti-pseudomonas agents we tested, supporting an idea that these RND-type multidrug efflux transporters are molecular targets to overcome multidrug resistance in P aeruginosa. mexEF-oprN-upregulation in P aeruginosa PA7 was shown due to a MexS variant harboring the Valine-155 amino acid residue. This is the first genetic evidence shown that a MexS variant causes mexEF-oprN-upregulation in P aeruginosa clinical isolates.
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