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SOS Response Induces Persistence to Fluoroquinolones in Escherichia coli

Bacteria can survive antibiotic treatment without acquiring heritable antibiotic resistance. We investigated persistence to the fluoroquinolone ciprofloxacin in Escherichia coli. Our data show that a majority of persisters to ciprofloxacin were formed upon exposure to the antibiotic, in a manner dep...

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Detalles Bibliográficos
Autores principales: Dörr, Tobias, Lewis, Kim, Vulić, Marin
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780357/
https://www.ncbi.nlm.nih.gov/pubmed/20011100
http://dx.doi.org/10.1371/journal.pgen.1000760
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author Dörr, Tobias
Lewis, Kim
Vulić, Marin
author_facet Dörr, Tobias
Lewis, Kim
Vulić, Marin
author_sort Dörr, Tobias
collection PubMed
description Bacteria can survive antibiotic treatment without acquiring heritable antibiotic resistance. We investigated persistence to the fluoroquinolone ciprofloxacin in Escherichia coli. Our data show that a majority of persisters to ciprofloxacin were formed upon exposure to the antibiotic, in a manner dependent on the SOS gene network. These findings reveal an active and inducible mechanism of persister formation mediated by the SOS response, challenging the prevailing view that persisters are pre-existing and formed purely by stochastic means. SOS-induced persistence is a novel mechanism by which cells can counteract DNA damage and promote survival to fluoroquinolones. This unique survival mechanism may be an important factor influencing the outcome of antibiotic therapy in vivo.
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spelling pubmed-27803572009-12-15 SOS Response Induces Persistence to Fluoroquinolones in Escherichia coli Dörr, Tobias Lewis, Kim Vulić, Marin PLoS Genet Research Article Bacteria can survive antibiotic treatment without acquiring heritable antibiotic resistance. We investigated persistence to the fluoroquinolone ciprofloxacin in Escherichia coli. Our data show that a majority of persisters to ciprofloxacin were formed upon exposure to the antibiotic, in a manner dependent on the SOS gene network. These findings reveal an active and inducible mechanism of persister formation mediated by the SOS response, challenging the prevailing view that persisters are pre-existing and formed purely by stochastic means. SOS-induced persistence is a novel mechanism by which cells can counteract DNA damage and promote survival to fluoroquinolones. This unique survival mechanism may be an important factor influencing the outcome of antibiotic therapy in vivo. Public Library of Science 2009-12-11 /pmc/articles/PMC2780357/ /pubmed/20011100 http://dx.doi.org/10.1371/journal.pgen.1000760 Text en Dörr et al. http://creativecommons.org/licenses/by/4.0/ 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 properly credited.
spellingShingle Research Article
Dörr, Tobias
Lewis, Kim
Vulić, Marin
SOS Response Induces Persistence to Fluoroquinolones in Escherichia coli
title SOS Response Induces Persistence to Fluoroquinolones in Escherichia coli
title_full SOS Response Induces Persistence to Fluoroquinolones in Escherichia coli
title_fullStr SOS Response Induces Persistence to Fluoroquinolones in Escherichia coli
title_full_unstemmed SOS Response Induces Persistence to Fluoroquinolones in Escherichia coli
title_short SOS Response Induces Persistence to Fluoroquinolones in Escherichia coli
title_sort sos response induces persistence to fluoroquinolones in escherichia coli
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2780357/
https://www.ncbi.nlm.nih.gov/pubmed/20011100
http://dx.doi.org/10.1371/journal.pgen.1000760
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