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Persistence of obligate intracellular pathogens: alternative strategies to overcome host-specific stresses

In adapting to the intracellular niche, obligate intracellular bacteria usually undergo a reduction of genome size by eliminating genes not needed for intracellular survival. These losses can include, for example, genes involved in nutrient anabolic pathways or in stress response. Living inside a ho...

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Autores principales: Riffaud, Camille M., Rucks, Elizabeth A., Ouellette, Scot P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10239878/
https://www.ncbi.nlm.nih.gov/pubmed/37284502
http://dx.doi.org/10.3389/fcimb.2023.1185571
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author Riffaud, Camille M.
Rucks, Elizabeth A.
Ouellette, Scot P.
author_facet Riffaud, Camille M.
Rucks, Elizabeth A.
Ouellette, Scot P.
author_sort Riffaud, Camille M.
collection PubMed
description In adapting to the intracellular niche, obligate intracellular bacteria usually undergo a reduction of genome size by eliminating genes not needed for intracellular survival. These losses can include, for example, genes involved in nutrient anabolic pathways or in stress response. Living inside a host cell offers a stable environment where intracellular bacteria can limit their exposure to extracellular effectors of the immune system and modulate or outright inhibit intracellular defense mechanisms. However, highlighting an area of vulnerability, these pathogens are dependent on the host cell for nutrients and are very sensitive to conditions that limit nutrient availability. Persistence is a common response shared by evolutionarily divergent bacteria to survive adverse conditions like nutrient deprivation. Development of persistence usually compromises successful antibiotic therapy of bacterial infections and is associated with chronic infections and long-term sequelae for the patients. During persistence, obligate intracellular pathogens are viable but not growing inside their host cell. They can survive for a long period of time such that, when the inducing stress is removed, reactivation of their growth cycles resumes. Given their reduced coding capacity, intracellular bacteria have adapted different response mechanisms. This review gives an overview of the strategies used by the obligate intracellular bacteria, where known, which, unlike model organisms such as E. coli, often lack toxin-antitoxin systems and the stringent response that have been linked to a persister phenotype and amino acid starvation states, respectively.
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spelling pubmed-102398782023-06-06 Persistence of obligate intracellular pathogens: alternative strategies to overcome host-specific stresses Riffaud, Camille M. Rucks, Elizabeth A. Ouellette, Scot P. Front Cell Infect Microbiol Cellular and Infection Microbiology In adapting to the intracellular niche, obligate intracellular bacteria usually undergo a reduction of genome size by eliminating genes not needed for intracellular survival. These losses can include, for example, genes involved in nutrient anabolic pathways or in stress response. Living inside a host cell offers a stable environment where intracellular bacteria can limit their exposure to extracellular effectors of the immune system and modulate or outright inhibit intracellular defense mechanisms. However, highlighting an area of vulnerability, these pathogens are dependent on the host cell for nutrients and are very sensitive to conditions that limit nutrient availability. Persistence is a common response shared by evolutionarily divergent bacteria to survive adverse conditions like nutrient deprivation. Development of persistence usually compromises successful antibiotic therapy of bacterial infections and is associated with chronic infections and long-term sequelae for the patients. During persistence, obligate intracellular pathogens are viable but not growing inside their host cell. They can survive for a long period of time such that, when the inducing stress is removed, reactivation of their growth cycles resumes. Given their reduced coding capacity, intracellular bacteria have adapted different response mechanisms. This review gives an overview of the strategies used by the obligate intracellular bacteria, where known, which, unlike model organisms such as E. coli, often lack toxin-antitoxin systems and the stringent response that have been linked to a persister phenotype and amino acid starvation states, respectively. Frontiers Media S.A. 2023-05-22 /pmc/articles/PMC10239878/ /pubmed/37284502 http://dx.doi.org/10.3389/fcimb.2023.1185571 Text en Copyright © 2023 Riffaud, Rucks and Ouellette https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cellular and Infection Microbiology
Riffaud, Camille M.
Rucks, Elizabeth A.
Ouellette, Scot P.
Persistence of obligate intracellular pathogens: alternative strategies to overcome host-specific stresses
title Persistence of obligate intracellular pathogens: alternative strategies to overcome host-specific stresses
title_full Persistence of obligate intracellular pathogens: alternative strategies to overcome host-specific stresses
title_fullStr Persistence of obligate intracellular pathogens: alternative strategies to overcome host-specific stresses
title_full_unstemmed Persistence of obligate intracellular pathogens: alternative strategies to overcome host-specific stresses
title_short Persistence of obligate intracellular pathogens: alternative strategies to overcome host-specific stresses
title_sort persistence of obligate intracellular pathogens: alternative strategies to overcome host-specific stresses
topic Cellular and Infection Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10239878/
https://www.ncbi.nlm.nih.gov/pubmed/37284502
http://dx.doi.org/10.3389/fcimb.2023.1185571
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