Modern Acinetobacter baumannii clinical isolates replicate inside spacious vacuoles and egress from macrophages.

Multidrug-resistant Acinetobacter baumannii infections are increasing at alarming rates. Therefore, novel antibiotic-sparing treatments to combat these A. baumannii infections are urgently needed. The development of these interventions would benefit from a better understanding of this bacterium'...

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Autores principales: Gabriela Sycz, Gisela Di Venanzio, Jesus S Distel, Mariana G Sartorio, Nguyen-Hung Le, Nichollas E Scott, Wandy L Beatty, Mario F Feldman
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Publicado: Public Library of Science (PLoS) 2021
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Acceso en línea:https://doaj.org/article/d09b4c9b97c44eaaab6d066fa2a98b86
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spelling oai:doaj.org-article:d09b4c9b97c44eaaab6d066fa2a98b862021-12-02T20:00:24ZModern Acinetobacter baumannii clinical isolates replicate inside spacious vacuoles and egress from macrophages.1553-73661553-737410.1371/journal.ppat.1009802https://doaj.org/article/d09b4c9b97c44eaaab6d066fa2a98b862021-08-01T00:00:00Zhttps://doi.org/10.1371/journal.ppat.1009802https://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Multidrug-resistant Acinetobacter baumannii infections are increasing at alarming rates. Therefore, novel antibiotic-sparing treatments to combat these A. baumannii infections are urgently needed. The development of these interventions would benefit from a better understanding of this bacterium's pathobiology, which remains poorly understood. A. baumannii is regarded as an extracellular opportunistic pathogen. However, research on Acinetobacter has largely focused on common lab strains, such as ATCC 19606, that have been isolated several decades ago. These strains exhibit reduced virulence when compared to recently isolated clinical strains. In this work, we demonstrate that, unlike ATCC 19606, several modern A. baumannii clinical isolates, including the recent clinical urinary isolate UPAB1, persist and replicate inside macrophages within spacious vacuoles. We show that intracellular replication of UPAB1 is dependent on a functional type I secretion system (T1SS) and pAB5, a large conjugative plasmid that controls the expression of several chromosomally-encoded genes. Finally, we show that UPAB1 escapes from the infected macrophages by a lytic process. To our knowledge, this is the first report of intracellular growth and replication of A. baumannii. We suggest that intracellular replication within macrophages may contribute to evasion of the immune response, dissemination, and antibiotic tolerance of A. baumannii.Gabriela SyczGisela Di VenanzioJesus S DistelMariana G SartorioNguyen-Hung LeNichollas E ScottWandy L BeattyMario F FeldmanPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 17, Iss 8, p e1009802 (2021)
institution DOAJ
collection DOAJ
language EN
topic Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
spellingShingle Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
Gabriela Sycz
Gisela Di Venanzio
Jesus S Distel
Mariana G Sartorio
Nguyen-Hung Le
Nichollas E Scott
Wandy L Beatty
Mario F Feldman
Modern Acinetobacter baumannii clinical isolates replicate inside spacious vacuoles and egress from macrophages.
description Multidrug-resistant Acinetobacter baumannii infections are increasing at alarming rates. Therefore, novel antibiotic-sparing treatments to combat these A. baumannii infections are urgently needed. The development of these interventions would benefit from a better understanding of this bacterium's pathobiology, which remains poorly understood. A. baumannii is regarded as an extracellular opportunistic pathogen. However, research on Acinetobacter has largely focused on common lab strains, such as ATCC 19606, that have been isolated several decades ago. These strains exhibit reduced virulence when compared to recently isolated clinical strains. In this work, we demonstrate that, unlike ATCC 19606, several modern A. baumannii clinical isolates, including the recent clinical urinary isolate UPAB1, persist and replicate inside macrophages within spacious vacuoles. We show that intracellular replication of UPAB1 is dependent on a functional type I secretion system (T1SS) and pAB5, a large conjugative plasmid that controls the expression of several chromosomally-encoded genes. Finally, we show that UPAB1 escapes from the infected macrophages by a lytic process. To our knowledge, this is the first report of intracellular growth and replication of A. baumannii. We suggest that intracellular replication within macrophages may contribute to evasion of the immune response, dissemination, and antibiotic tolerance of A. baumannii.
format article
author Gabriela Sycz
Gisela Di Venanzio
Jesus S Distel
Mariana G Sartorio
Nguyen-Hung Le
Nichollas E Scott
Wandy L Beatty
Mario F Feldman
author_facet Gabriela Sycz
Gisela Di Venanzio
Jesus S Distel
Mariana G Sartorio
Nguyen-Hung Le
Nichollas E Scott
Wandy L Beatty
Mario F Feldman
author_sort Gabriela Sycz
title Modern Acinetobacter baumannii clinical isolates replicate inside spacious vacuoles and egress from macrophages.
title_short Modern Acinetobacter baumannii clinical isolates replicate inside spacious vacuoles and egress from macrophages.
title_full Modern Acinetobacter baumannii clinical isolates replicate inside spacious vacuoles and egress from macrophages.
title_fullStr Modern Acinetobacter baumannii clinical isolates replicate inside spacious vacuoles and egress from macrophages.
title_full_unstemmed Modern Acinetobacter baumannii clinical isolates replicate inside spacious vacuoles and egress from macrophages.
title_sort modern acinetobacter baumannii clinical isolates replicate inside spacious vacuoles and egress from macrophages.
publisher Public Library of Science (PLoS)
publishDate 2021
url https://doaj.org/article/d09b4c9b97c44eaaab6d066fa2a98b86
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