A Quorum Sensing Small Volatile Molecule Promotes Antibiotic Tolerance in Bacteria

Bacteria can be refractory to antibiotics due to a sub-population of dormant cells, called persisters that are highly tolerant to antibiotic exposure. The low frequency and transience of the antibiotic tolerant “persister” trait has complicated elucidation of the mechanism that controls antibiotic t...

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Main Authors: Que, Yok-Ai, Hazan, Ronen, Strobel, Benjamin, Maura, Damien, He, Jianxin, Kesarwani, Meenu, Panopoulos, Panagiotis, Tsurumi, Amy, Giddey, Marlyse, Wilhelmy, Julie, Mindrinos, Michael N., Rahme, Laurence G.
Format: Online
Language:English
Published: Public Library of Science 2013
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3868577/
id pubmed-3868577
recordtype oai_dc
spelling pubmed-38685772013-12-23 A Quorum Sensing Small Volatile Molecule Promotes Antibiotic Tolerance in Bacteria Que, Yok-Ai Hazan, Ronen Strobel, Benjamin Maura, Damien He, Jianxin Kesarwani, Meenu Panopoulos, Panagiotis Tsurumi, Amy Giddey, Marlyse Wilhelmy, Julie Mindrinos, Michael N. Rahme, Laurence G. Research Article Bacteria can be refractory to antibiotics due to a sub-population of dormant cells, called persisters that are highly tolerant to antibiotic exposure. The low frequency and transience of the antibiotic tolerant “persister” trait has complicated elucidation of the mechanism that controls antibiotic tolerance. In this study, we show that 2’ Amino-acetophenone (2-AA), a poorly studied but diagnostically important small, volatile molecule produced by the recalcitrant gram-negative human pathogen Pseudomonas aeruginosa, promotes antibiotic tolerance in response to quorum-sensing (QS) signaling. Our results show that 2-AA mediated persister cell accumulation occurs via alteration of the expression of genes involved in the translational capacity of the cell, including almost all ribosomal protein genes and other translation-related factors. That 2-AA promotes persisters formation also in other emerging multi-drug resistant pathogens, including the non 2-AA producer Acinetobacter baumannii implies that 2-AA may play an important role in the ability of gram-negative bacteria to tolerate antibiotic treatments in polymicrobial infections. Given that the synthesis, excretion and uptake of QS small molecules is a common hallmark of prokaryotes, together with the fact that the translational machinery is highly conserved, we posit that modulation of the translational capacity of the cell via QS molecules, may be a general, widely distributed mechanism that promotes antibiotic tolerance among prokaryotes. Public Library of Science 2013-12-19 /pmc/articles/PMC3868577/ /pubmed/24367477 http://dx.doi.org/10.1371/journal.pone.0080140 Text en © 2013 Que 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.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Que, Yok-Ai
Hazan, Ronen
Strobel, Benjamin
Maura, Damien
He, Jianxin
Kesarwani, Meenu
Panopoulos, Panagiotis
Tsurumi, Amy
Giddey, Marlyse
Wilhelmy, Julie
Mindrinos, Michael N.
Rahme, Laurence G.
spellingShingle Que, Yok-Ai
Hazan, Ronen
Strobel, Benjamin
Maura, Damien
He, Jianxin
Kesarwani, Meenu
Panopoulos, Panagiotis
Tsurumi, Amy
Giddey, Marlyse
Wilhelmy, Julie
Mindrinos, Michael N.
Rahme, Laurence G.
A Quorum Sensing Small Volatile Molecule Promotes Antibiotic Tolerance in Bacteria
author_facet Que, Yok-Ai
Hazan, Ronen
Strobel, Benjamin
Maura, Damien
He, Jianxin
Kesarwani, Meenu
Panopoulos, Panagiotis
Tsurumi, Amy
Giddey, Marlyse
Wilhelmy, Julie
Mindrinos, Michael N.
Rahme, Laurence G.
author_sort Que, Yok-Ai
title A Quorum Sensing Small Volatile Molecule Promotes Antibiotic Tolerance in Bacteria
title_short A Quorum Sensing Small Volatile Molecule Promotes Antibiotic Tolerance in Bacteria
title_full A Quorum Sensing Small Volatile Molecule Promotes Antibiotic Tolerance in Bacteria
title_fullStr A Quorum Sensing Small Volatile Molecule Promotes Antibiotic Tolerance in Bacteria
title_full_unstemmed A Quorum Sensing Small Volatile Molecule Promotes Antibiotic Tolerance in Bacteria
title_sort quorum sensing small volatile molecule promotes antibiotic tolerance in bacteria
description Bacteria can be refractory to antibiotics due to a sub-population of dormant cells, called persisters that are highly tolerant to antibiotic exposure. The low frequency and transience of the antibiotic tolerant “persister” trait has complicated elucidation of the mechanism that controls antibiotic tolerance. In this study, we show that 2’ Amino-acetophenone (2-AA), a poorly studied but diagnostically important small, volatile molecule produced by the recalcitrant gram-negative human pathogen Pseudomonas aeruginosa, promotes antibiotic tolerance in response to quorum-sensing (QS) signaling. Our results show that 2-AA mediated persister cell accumulation occurs via alteration of the expression of genes involved in the translational capacity of the cell, including almost all ribosomal protein genes and other translation-related factors. That 2-AA promotes persisters formation also in other emerging multi-drug resistant pathogens, including the non 2-AA producer Acinetobacter baumannii implies that 2-AA may play an important role in the ability of gram-negative bacteria to tolerate antibiotic treatments in polymicrobial infections. Given that the synthesis, excretion and uptake of QS small molecules is a common hallmark of prokaryotes, together with the fact that the translational machinery is highly conserved, we posit that modulation of the translational capacity of the cell via QS molecules, may be a general, widely distributed mechanism that promotes antibiotic tolerance among prokaryotes.
publisher Public Library of Science
publishDate 2013
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3868577/
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