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Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells

Pseudomonas aeruginosa is a ubiquitous environmental organism and an opportunistic pathogen that causes chronic lung infections in the airways of cystic fibrosis (CF) patients as well as other immune-compromised individuals. During infection, P. aeruginosa enters the terminal bronchioles and alveoli...

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Autores principales: Hill, Preston J., Scordo, Julia M., Arcos, Jesús, Kirkby, Stephen E., Wewers, Mark D., Wozniak, Daniel J., Torrelles, Jordi B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5500645/
https://www.ncbi.nlm.nih.gov/pubmed/28684799
http://dx.doi.org/10.1038/s41598-017-05253-9
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author Hill, Preston J.
Scordo, Julia M.
Arcos, Jesús
Kirkby, Stephen E.
Wewers, Mark D.
Wozniak, Daniel J.
Torrelles, Jordi B.
author_facet Hill, Preston J.
Scordo, Julia M.
Arcos, Jesús
Kirkby, Stephen E.
Wewers, Mark D.
Wozniak, Daniel J.
Torrelles, Jordi B.
author_sort Hill, Preston J.
collection PubMed
description Pseudomonas aeruginosa is a ubiquitous environmental organism and an opportunistic pathogen that causes chronic lung infections in the airways of cystic fibrosis (CF) patients as well as other immune-compromised individuals. During infection, P. aeruginosa enters the terminal bronchioles and alveoli and comes into contact with alveolar lining fluid (ALF), which contains homeostatic and antimicrobial hydrolytic activities, termed hydrolases. These hydrolases comprise an array of lipases, glycosidases, and proteases and thus, they have the potential to modify lipids, carbohydrates and proteins on the surface of invading microbes. Here we show that hydrolase levels between human ALF from healthy and CF patients differ. CF-ALF influences the P. aeruginosa cell wall by reducing the content of one of its major polysaccharides, Psl. This CF-ALF induced Psl reduction does not alter initial bacterial attachment to surfaces but reduces biofilm formation. Importantly, exposure of P. aeruginosa to CF-ALF drives the activation of neutrophils and triggers their oxidative response; thus, defining human CF-ALF as a new innate defense mechanism to control P. aeruginosa infection, but at the same time potentially adding to the chronic inflammatory state of the lung in CF patients.
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spelling pubmed-55006452017-07-10 Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells Hill, Preston J. Scordo, Julia M. Arcos, Jesús Kirkby, Stephen E. Wewers, Mark D. Wozniak, Daniel J. Torrelles, Jordi B. Sci Rep Article Pseudomonas aeruginosa is a ubiquitous environmental organism and an opportunistic pathogen that causes chronic lung infections in the airways of cystic fibrosis (CF) patients as well as other immune-compromised individuals. During infection, P. aeruginosa enters the terminal bronchioles and alveoli and comes into contact with alveolar lining fluid (ALF), which contains homeostatic and antimicrobial hydrolytic activities, termed hydrolases. These hydrolases comprise an array of lipases, glycosidases, and proteases and thus, they have the potential to modify lipids, carbohydrates and proteins on the surface of invading microbes. Here we show that hydrolase levels between human ALF from healthy and CF patients differ. CF-ALF influences the P. aeruginosa cell wall by reducing the content of one of its major polysaccharides, Psl. This CF-ALF induced Psl reduction does not alter initial bacterial attachment to surfaces but reduces biofilm formation. Importantly, exposure of P. aeruginosa to CF-ALF drives the activation of neutrophils and triggers their oxidative response; thus, defining human CF-ALF as a new innate defense mechanism to control P. aeruginosa infection, but at the same time potentially adding to the chronic inflammatory state of the lung in CF patients. Nature Publishing Group UK 2017-07-06 /pmc/articles/PMC5500645/ /pubmed/28684799 http://dx.doi.org/10.1038/s41598-017-05253-9 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Hill, Preston J.
Scordo, Julia M.
Arcos, Jesús
Kirkby, Stephen E.
Wewers, Mark D.
Wozniak, Daniel J.
Torrelles, Jordi B.
Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells
title Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells
title_full Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells
title_fullStr Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells
title_full_unstemmed Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells
title_short Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells
title_sort modifications of pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5500645/
https://www.ncbi.nlm.nih.gov/pubmed/28684799
http://dx.doi.org/10.1038/s41598-017-05253-9
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