期刊
ISME JOURNAL
卷 6, 期 3, 页码 493-501出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ismej.2011.122
关键词
drug resistance; efflux pump; Pseudomonas aeruginosa; quorum sensing; quorum quenching
资金
- NIH [R01 GM089999]
- Japan Society for the Promotion of Science
- SEP/CONACyT [152794]
Quorum sensing (QS) is the regulation of gene expression in response to the concentration of small signal molecules, and its inactivation has been suggested to have great potential to attenuate microbial virulence. It is assumed that unlike antimicrobials, inhibition of QS should cause less Darwinian selection pressure for bacterial resistance. Using the opportunistic pathogen Pseudomonas aeruginosa, we demonstrate here that bacterial resistance arises rapidly to the best-characterized compound that inhibits QS (brominated furanone C-30) due to mutations that increase the efflux of C-30. Critically, the C-30-resistant mutant mexR was more pathogenic to Caenorhabditis elegans in the presence of C-30, and the same mutation arises in bacteria responsible for chronic cystic fibrosis infections. Therefore, bacteria may evolve resistance to many new pharmaceuticals thought impervious to resistance. The ISME Journal (2012) 6, 493-501; doi: 10.1038/ismej.2011.122; published online 15 September 2011
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