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

Abstract 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 an...

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Autores principales:	Preston J. Hill, Julia M. Scordo, Jesús Arcos, Stephen E. Kirkby, Mark D. Wewers, Daniel J. Wozniak, Jordi B. Torrelles
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b1443aee4d644607bb0dda7871f95373
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spelling	oai:doaj.org-article:b1443aee4d644607bb0dda7871f953732021-12-02T11:40:31ZModifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells10.1038/s41598-017-05253-92045-2322https://doaj.org/article/b1443aee4d644607bb0dda7871f953732017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-05253-9https://doaj.org/toc/2045-2322Abstract 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.Preston J. HillJulia M. ScordoJesús ArcosStephen E. KirkbyMark D. WewersDaniel J. WozniakJordi B. TorrellesNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Preston J. Hill Julia M. Scordo Jesús Arcos Stephen E. Kirkby Mark D. Wewers Daniel J. Wozniak Jordi B. Torrelles Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells
description	Abstract 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.
format	article
author	Preston J. Hill Julia M. Scordo Jesús Arcos Stephen E. Kirkby Mark D. Wewers Daniel J. Wozniak Jordi B. Torrelles
author_facet	Preston J. Hill Julia M. Scordo Jesús Arcos Stephen E. Kirkby Mark D. Wewers Daniel J. Wozniak Jordi B. Torrelles
author_sort	Preston J. Hill
title	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_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_sort	modifications of pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/b1443aee4d644607bb0dda7871f95373
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Modifications of Pseudomonas aeruginosa cell envelope in the cystic fibrosis airway alters interactions with immune cells

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