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Pseudomonas aeruginosa Consumption of Airway Metabolites Promotes Lung Infection
Prevailing dogma indicates that the lung of cystic fibrosis (CF) individuals is infected by multiple pathogens due to the abundant accumulation of mucus, which traps most of inhaled organisms. However, this hypothesis does not explain how specific opportunists, like Pseudomonas aeruginosa, are selec...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8401524/ https://www.ncbi.nlm.nih.gov/pubmed/34451421 http://dx.doi.org/10.3390/pathogens10080957 |
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author | Riquelme, Sebastián A. Prince, Alice |
author_facet | Riquelme, Sebastián A. Prince, Alice |
author_sort | Riquelme, Sebastián A. |
collection | PubMed |
description | Prevailing dogma indicates that the lung of cystic fibrosis (CF) individuals is infected by multiple pathogens due to the abundant accumulation of mucus, which traps most of inhaled organisms. However, this hypothesis does not explain how specific opportunists, like Pseudomonas aeruginosa, are selected in the CF lung to cause chronic disease. This strongly suggests that other factors than mucus are accrued in the human airway and might predispose to bacterial disease, especially by P. aeruginosa. In this review we discuss the role of macrophage metabolites, like succinate and itaconate, in P. aeruginosa pneumonia. We analyze how dysfunction of the CF transmembrane conductance regulator (CFTR) favors release of these metabolites into the infected airway, and how P. aeruginosa exploits these elements to induce transcriptomic and metabolic changes that increase its capacity to cause intractable disease. We describe the host and pathogen pathways associated with succinate and itaconate catabolism, mechanisms of bacterial adaptation to these determinants, and suggest how both experimental settings and future therapies should consider macrophage metabolites abundance to better study P. aeruginosa pathogenesis. |
format | Online Article Text |
id | pubmed-8401524 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-84015242021-08-29 Pseudomonas aeruginosa Consumption of Airway Metabolites Promotes Lung Infection Riquelme, Sebastián A. Prince, Alice Pathogens Review Prevailing dogma indicates that the lung of cystic fibrosis (CF) individuals is infected by multiple pathogens due to the abundant accumulation of mucus, which traps most of inhaled organisms. However, this hypothesis does not explain how specific opportunists, like Pseudomonas aeruginosa, are selected in the CF lung to cause chronic disease. This strongly suggests that other factors than mucus are accrued in the human airway and might predispose to bacterial disease, especially by P. aeruginosa. In this review we discuss the role of macrophage metabolites, like succinate and itaconate, in P. aeruginosa pneumonia. We analyze how dysfunction of the CF transmembrane conductance regulator (CFTR) favors release of these metabolites into the infected airway, and how P. aeruginosa exploits these elements to induce transcriptomic and metabolic changes that increase its capacity to cause intractable disease. We describe the host and pathogen pathways associated with succinate and itaconate catabolism, mechanisms of bacterial adaptation to these determinants, and suggest how both experimental settings and future therapies should consider macrophage metabolites abundance to better study P. aeruginosa pathogenesis. MDPI 2021-07-29 /pmc/articles/PMC8401524/ /pubmed/34451421 http://dx.doi.org/10.3390/pathogens10080957 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Riquelme, Sebastián A. Prince, Alice Pseudomonas aeruginosa Consumption of Airway Metabolites Promotes Lung Infection |
title | Pseudomonas aeruginosa Consumption of Airway Metabolites Promotes Lung Infection |
title_full | Pseudomonas aeruginosa Consumption of Airway Metabolites Promotes Lung Infection |
title_fullStr | Pseudomonas aeruginosa Consumption of Airway Metabolites Promotes Lung Infection |
title_full_unstemmed | Pseudomonas aeruginosa Consumption of Airway Metabolites Promotes Lung Infection |
title_short | Pseudomonas aeruginosa Consumption of Airway Metabolites Promotes Lung Infection |
title_sort | pseudomonas aeruginosa consumption of airway metabolites promotes lung infection |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8401524/ https://www.ncbi.nlm.nih.gov/pubmed/34451421 http://dx.doi.org/10.3390/pathogens10080957 |
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