Journal ArticleDOI
Antibiotic persistence and tolerance: not just one and the same.
TLDR
In this paper, the authors discuss the current understanding of antibiotic tolerance and persistence, outlining how tolerance and persistent can be distinguished experimentally, and evaluate the clinical evidence implicating antibiotic tolerance in recalcitrance and relapse of bacterial infections.About:
This article is published in Current Opinion in Microbiology.The article was published on 2021-12-01. It has received 18 citations till now. The article focuses on the topics: Population & Multidrug tolerance.read more
Citations
More filters
Journal ArticleDOI
An Isotope-Labeled Single-Cell Raman Spectroscopy Approach for Tracking the Physiological Evolution Trajectory of Bacteria toward Antibiotic Resistance.
TL;DR: In this article , a single-cell approach integrating D2O-labeled Raman spectroscopy, advanced multivariate analysis, and genotypic profiling is presented to in situ track physiological evolution trajectory toward resistance.
Journal ArticleDOI
Anti-persister strategies against stress induced bacterial persistence.
TL;DR: In this article , the detailed molecular mechanisms and strategies of bacterial persistence, including toxin-antitoxin modules, DNA damage, formation of inactive ribosomal complexes, (p)ppGpp network, antibiotic-induced persistence, which are triggered by drug-induced stress.
Journal ArticleDOI
Antibiotic tolerance and persistence have distinct fitness trade-offs
TL;DR: In this article , the authors show that antibiotic tolerance can be achieved in numerous non-specific ways in vitro and during infection, and highlight that due to their impact on the entire bacterial population, these tolerance-inducing conditions completely mask persistence and the action of its molecular determinants.
Journal ArticleDOI
A DNA-Damage Inducible Gene Promotes the Formation of Antibiotic Persisters in Response to the Quorum Sensing Signaling Peptide in Streptococcus mutans
TL;DR: This study suggests that the pep299 gene is at the core of the triggered persistence phenotype in S. mutans, allowing cells to transition into a state of reduced metabolic activity and antibiotic tolerance.
Posted ContentDOI
Escherichia coli cells are primed for survival before lethal antibiotic stress
TL;DR: In this article , a modified Luria-Delbrück fluctuation test was used to explore whether a population of bacterial cells in a population, referred to as persister cells, tolerate long-term lethal antibiotic effects by entering into a non-dividing, metabolically altered state.
References
More filters
Journal ArticleDOI
Bacterial Persistence as a Phenotypic Switch
Nathalie Q. Balaban,Nathalie Q. Balaban,Jack Merrin,Remy Chait,Lukasz Kowalik,Stanislas Leibler +5 more
TL;DR: Investigating the persistence of single cells of Escherichia coli with the use of microfluidic devices found phenotypic switching occurred between normally growing cells and persister cells having reduced growth rates, leading to a simple mathematical description of the persistence switch.
Journal ArticleDOI
Persister cells and tolerance to antimicrobials.
TL;DR: The data indicate that persisters are specialized survivor cells that are not at a particular stage in the cell cycle, neither are they defective cells nor cells created in response to antibiotics.
Journal ArticleDOI
Residual guanosine 3',5'-bispyrophosphate synthetic activity of relA null mutants can be eliminated by spoT null mutations.
TL;DR: It is proposed that the SpoT protein can either catalyze or control the alternative pathway of ppGpp synthesis in addition to its known role as a (p)ppGpp 3'-pyrophosphohydrolase.
Journal ArticleDOI
RAD51B in Familial Breast Cancer
Liisa M. Pelttari,Sofia Khan,Mikko Vuorela,Johanna I. Kiiski,Sara Vilske,Viivi Nevanlinna,Salla Ranta,Johanna Schleutker,Johanna Schleutker,Johanna Schleutker,Robert Winqvist,Anne Kallioniemi,Thilo Dörk,Natalia Bogdanova,Jonine Figueroa,Paul D.P. Pharoah,Marjanka K. Schmidt,Alison M. Dunning,Montserrat Garcia-Closas,Manjeet K. Bolla,Joe Dennis,Kyriaki Michailidou,Qin Wang,John L. Hopper,Melissa C. Southey,Efraim H. Rosenberg,Peter A. Fasching,Peter A. Fasching,Matthias W. Beckmann,Julian Peto,Isabel dos-Santos-Silva,Elinor J. Sawyer,Ian Tomlinson,Barbara Burwinkel,Barbara Burwinkel,Harald Surowy,Harald Surowy,Pascal Guénel,Thérèse Truong,Stig E. Bojesen,Stig E. Bojesen,Børge G. Nordestgaard,Børge G. Nordestgaard,Javier Benitez,Anna González-Neira,Susan L. Neuhausen,Hoda Anton-Culver,Hermann Brenner,Volker Arndt,Alfons Meindl,Rita K. Schmutzler,Hiltrud Brauch,Hiltrud Brauch,Hiltrud Brauch,Thomas Brüning,Annika Lindblom,Sara Margolin,Arto Mannermaa,Jaana M. Hartikainen,Georgia Chenevix-Trench,kConFab,kConFab,Aocs Investigators,Laurien Van Dyck,Hilde Janssen,Hilde Janssen,Jenny Chang-Claude,Anja Rudolph,Paolo Radice,Paolo Peterlongo,Emily Hallberg,Janet E. Olson,Janet E. Olson,Graham G. Giles,Graham G. Giles,Roger L. Milne,Christopher A. Haiman,Fredrick Schumacher,Jacques Simard,Martine Dumont,Martine Dumont,Vessela N. Kristensen,Vessela N. Kristensen,Anne Lise Børresen-Dale,Wei Zheng,Alicia Beeghly-Fadiel,Mervi Grip,Mervi Grip,Irene L. Andrulis,Gord Glendon,Peter Devilee,Caroline Seynaeve,Maartje J. Hooning,Margriet Collée,Angela Cox,Simon S. Cross,Mitul Shah,Robert Luben,Ute Hamann,Ute Hamann,Diana Torres,Anna Jakubowska,Jan Lubinski,Fergus J. Couch,Drakoulis Yannoukakos,Nick Orr,Anthony J. Swerdlow,Hatef Darabi,Jingmei Li,Kamila Czene,Per Hall,Douglas F. Easton,Johanna Mattson,Carl Blomqvist,Kristiina Aittomäki,Heli Nevanlinna +115 more
TL;DR: It is suggested that loss-of-function mutations in RAD 51B are rare, but common variation at the RAD51B region is significantly associated with familial breast cancer risk.
Journal ArticleDOI
Antibiotics induce redox-related physiological alterations as part of their lethality
Daniel J. Dwyer,Peter Belenky,Jason H. Yang,I. Cody MacDonald,Jeffrey D. Martell,Noriko Takahashi,Clement T Y Chan,Michael A. Lobritz,Dana Braff,Eric G. Schwarz,Jonathan D. Ye,Mekhala Pati,Maarten Vercruysse,Paul S. Ralifo,Kyle R. Allison,Ahmad S. Khalil,Alice Y. Ting,Graham C. Walker,James J. Collins +18 more
TL;DR: This work provides direct evidence that, downstream of their target-specific interactions, bactericidal antibiotics induce complex redox alterations that contribute to cellular damage and death, thus supporting an evolving, expanded model of antibiotic lethality.