<i>Pseudomonas aeruginosa</i> 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 <i>Pseudomonas aeruginosa&l...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2021-07-01
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| Series: | Pathogens |
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| Online Access: | https://www.mdpi.com/2076-0817/10/8/957 |
| _version_ | 1827684466790760448 |
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| author | Sebastián A. Riquelme Alice Prince |
| author_facet | Sebastián A. Riquelme Alice Prince |
| author_sort | Sebastián A. Riquelme |
| collection | DOAJ |
| 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 <i>Pseudomonas aeruginosa</i>, 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 <i>P. aeruginosa</i>. In this review we discuss the role of macrophage metabolites, like succinate and itaconate, in <i>P. aeruginosa</i> pneumonia. We analyze how dysfunction of the CF transmembrane conductance regulator (CFTR) favors release of these metabolites into the infected airway, and how <i>P. aeruginosa</i> 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 <i>P. aeruginosa</i> pathogenesis. |
| first_indexed | 2024-03-10T08:30:41Z |
| format | Article |
| id | doaj.art-df92062afff84cff880d904a6051946c |
| institution | Directory Open Access Journal |
| issn | 2076-0817 |
| language | English |
| last_indexed | 2024-03-10T08:30:41Z |
| publishDate | 2021-07-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Pathogens |
| spelling | doaj.art-df92062afff84cff880d904a6051946c2023-11-22T09:08:35ZengMDPI AGPathogens2076-08172021-07-0110895710.3390/pathogens10080957<i>Pseudomonas aeruginosa</i> Consumption of Airway Metabolites Promotes Lung InfectionSebastián A. Riquelme0Alice Prince1Department of Pediatrics, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USADepartment of Pediatrics, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USAPrevailing 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 <i>Pseudomonas aeruginosa</i>, 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 <i>P. aeruginosa</i>. In this review we discuss the role of macrophage metabolites, like succinate and itaconate, in <i>P. aeruginosa</i> pneumonia. We analyze how dysfunction of the CF transmembrane conductance regulator (CFTR) favors release of these metabolites into the infected airway, and how <i>P. aeruginosa</i> 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 <i>P. aeruginosa</i> pathogenesis.https://www.mdpi.com/2076-0817/10/8/957<i>Pseudomonas aeruginosa</i>immunometabolismsuccinateitaconatePTENCFTR |
| spellingShingle | Sebastián A. Riquelme Alice Prince <i>Pseudomonas aeruginosa</i> Consumption of Airway Metabolites Promotes Lung Infection Pathogens <i>Pseudomonas aeruginosa</i> immunometabolism succinate itaconate PTEN CFTR |
| title | <i>Pseudomonas aeruginosa</i> Consumption of Airway Metabolites Promotes Lung Infection |
| title_full | <i>Pseudomonas aeruginosa</i> Consumption of Airway Metabolites Promotes Lung Infection |
| title_fullStr | <i>Pseudomonas aeruginosa</i> Consumption of Airway Metabolites Promotes Lung Infection |
| title_full_unstemmed | <i>Pseudomonas aeruginosa</i> Consumption of Airway Metabolites Promotes Lung Infection |
| title_short | <i>Pseudomonas aeruginosa</i> Consumption of Airway Metabolites Promotes Lung Infection |
| title_sort | i pseudomonas aeruginosa i consumption of airway metabolites promotes lung infection |
| topic | <i>Pseudomonas aeruginosa</i> immunometabolism succinate itaconate PTEN CFTR |
| url | https://www.mdpi.com/2076-0817/10/8/957 |
| work_keys_str_mv | AT sebastianariquelme ipseudomonasaeruginosaiconsumptionofairwaymetabolitespromoteslunginfection AT aliceprince ipseudomonasaeruginosaiconsumptionofairwaymetabolitespromoteslunginfection |