A Physiological Basis for Nonheritable Antibiotic Resistance

ABSTRACT Antibiotics constitute one of the cornerstones of modern medicine. However, individuals may succumb to a bacterial infection if a pathogen survives exposure to antibiotics. The ability of bacteria to survive bactericidal antibiotics results from genetic changes in the preexisting bacterial...

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Autores principales:	Mauricio H. Pontes, Eduardo A. Groisman
Formato:	article
Lenguaje:	EN
Publicado:	American Society for Microbiology 2020
Materias:	antibiotic tolerance growth feedback regulation persister Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/86a2ddb2a6924515a6da0d2a453ecdd4
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id	oai:doaj.org-article:86a2ddb2a6924515a6da0d2a453ecdd4
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spelling	oai:doaj.org-article:86a2ddb2a6924515a6da0d2a453ecdd42021-11-15T15:56:47ZA Physiological Basis for Nonheritable Antibiotic Resistance10.1128/mBio.00817-202150-7511https://doaj.org/article/86a2ddb2a6924515a6da0d2a453ecdd42020-06-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mBio.00817-20https://doaj.org/toc/2150-7511ABSTRACT Antibiotics constitute one of the cornerstones of modern medicine. However, individuals may succumb to a bacterial infection if a pathogen survives exposure to antibiotics. The ability of bacteria to survive bactericidal antibiotics results from genetic changes in the preexisting bacterial genome, from the acquisition of genes from other organisms, and from nonheritable phenomena that give rise to antibiotic tolerance. Nonheritable antibiotic tolerance can be exhibited by a large fraction of the bacterial population or by a small subpopulation referred to as persisters. Nonheritable resistance to antibiotics has been ascribed to the activity of toxins that are part of toxin-antitoxin modules, to the universal energy currency ATP, and to the signaling molecule guanosine (penta) tetraphosphate. However, these molecules are dispensable for nonheritable resistance to antibiotics in many organisms. By contrast, nutrient limitation, treatment with bacteriostatic antibiotics, or expression of genes that slow bacterial growth invariably promote nonheritable resistance. We posit that antibiotic persistence results from conditions promoting feedback inhibition among core cellular processes, resulting phenotypically in a slowdown or halt in bacterial growth.Mauricio H. PontesEduardo A. GroismanAmerican Society for Microbiologyarticleantibiotic tolerancegrowth feedback regulationpersisterMicrobiologyQR1-502ENmBio, Vol 11, Iss 3 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	antibiotic tolerance growth feedback regulation persister Microbiology QR1-502
spellingShingle	antibiotic tolerance growth feedback regulation persister Microbiology QR1-502 Mauricio H. Pontes Eduardo A. Groisman A Physiological Basis for Nonheritable Antibiotic Resistance
description	ABSTRACT Antibiotics constitute one of the cornerstones of modern medicine. However, individuals may succumb to a bacterial infection if a pathogen survives exposure to antibiotics. The ability of bacteria to survive bactericidal antibiotics results from genetic changes in the preexisting bacterial genome, from the acquisition of genes from other organisms, and from nonheritable phenomena that give rise to antibiotic tolerance. Nonheritable antibiotic tolerance can be exhibited by a large fraction of the bacterial population or by a small subpopulation referred to as persisters. Nonheritable resistance to antibiotics has been ascribed to the activity of toxins that are part of toxin-antitoxin modules, to the universal energy currency ATP, and to the signaling molecule guanosine (penta) tetraphosphate. However, these molecules are dispensable for nonheritable resistance to antibiotics in many organisms. By contrast, nutrient limitation, treatment with bacteriostatic antibiotics, or expression of genes that slow bacterial growth invariably promote nonheritable resistance. We posit that antibiotic persistence results from conditions promoting feedback inhibition among core cellular processes, resulting phenotypically in a slowdown or halt in bacterial growth.
format	article
author	Mauricio H. Pontes Eduardo A. Groisman
author_facet	Mauricio H. Pontes Eduardo A. Groisman
author_sort	Mauricio H. Pontes
title	A Physiological Basis for Nonheritable Antibiotic Resistance
title_short	A Physiological Basis for Nonheritable Antibiotic Resistance
title_full	A Physiological Basis for Nonheritable Antibiotic Resistance
title_fullStr	A Physiological Basis for Nonheritable Antibiotic Resistance
title_full_unstemmed	A Physiological Basis for Nonheritable Antibiotic Resistance
title_sort	physiological basis for nonheritable antibiotic resistance
publisher	American Society for Microbiology
publishDate	2020
url	https://doaj.org/article/86a2ddb2a6924515a6da0d2a453ecdd4
work_keys_str_mv	AT mauriciohpontes aphysiologicalbasisfornonheritableantibioticresistance AT eduardoagroisman aphysiologicalbasisfornonheritableantibioticresistance AT mauriciohpontes physiologicalbasisfornonheritableantibioticresistance AT eduardoagroisman physiologicalbasisfornonheritableantibioticresistance
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A Physiological Basis for Nonheritable Antibiotic Resistance

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