A Pseudomonas aeruginosa toxin that hijacks the host ubiquitin proteolytic system.

Pseudomonas aeruginosa (P. aeruginosa) is an opportunistic pathogen chronically infecting the lungs of patients with chronic obstructive pulmonary disease (COPD), pneumonia, cystic fibrosis (CF), and bronchiectasis. Cif (PA2934), a bacterial toxin secreted in outer membrane vesicles (OMV) by P. aeru...

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Autores principales:	Jennifer M Bomberger, Siying Ye, Daniel P Maceachran, Katja Koeppen, Roxanna L Barnaby, George A O'Toole, Bruce A Stanton
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/056d8f81590b4b6a92ec79bf107cbb57
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spelling	oai:doaj.org-article:056d8f81590b4b6a92ec79bf107cbb572021-11-18T06:03:30ZA Pseudomonas aeruginosa toxin that hijacks the host ubiquitin proteolytic system.1553-73661553-737410.1371/journal.ppat.1001325https://doaj.org/article/056d8f81590b4b6a92ec79bf107cbb572011-03-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21455491/pdf/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Pseudomonas aeruginosa (P. aeruginosa) is an opportunistic pathogen chronically infecting the lungs of patients with chronic obstructive pulmonary disease (COPD), pneumonia, cystic fibrosis (CF), and bronchiectasis. Cif (PA2934), a bacterial toxin secreted in outer membrane vesicles (OMV) by P. aeruginosa, reduces CFTR-mediated chloride secretion by human airway epithelial cells, a key driving force for mucociliary clearance. The aim of this study was to investigate the mechanism whereby Cif reduces CFTR-mediated chloride secretion. Cif redirected endocytosed CFTR from recycling endosomes to lysosomes by stabilizing an inhibitory effect of G3BP1 on the deubiquitinating enzyme (DUB), USP10, thereby reducing USP10-mediated deubiquitination of CFTR and increasing the degradation of CFTR in lysosomes. This is the first example of a bacterial toxin that regulates the activity of a host DUB. These data suggest that the ability of P. aeruginosa to chronically infect the lungs of patients with COPD, pneumonia, CF, and bronchiectasis is due in part to the secretion of OMV containing Cif, which inhibits CFTR-mediated chloride secretion and thereby reduces the mucociliary clearance of pathogens.Jennifer M BombergerSiying YeDaniel P MaceachranKatja KoeppenRoxanna L BarnabyGeorge A O'TooleBruce A StantonPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 7, Iss 3, p e1001325 (2011)
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 Jennifer M Bomberger Siying Ye Daniel P Maceachran Katja Koeppen Roxanna L Barnaby George A O'Toole Bruce A Stanton A Pseudomonas aeruginosa toxin that hijacks the host ubiquitin proteolytic system.
description	Pseudomonas aeruginosa (P. aeruginosa) is an opportunistic pathogen chronically infecting the lungs of patients with chronic obstructive pulmonary disease (COPD), pneumonia, cystic fibrosis (CF), and bronchiectasis. Cif (PA2934), a bacterial toxin secreted in outer membrane vesicles (OMV) by P. aeruginosa, reduces CFTR-mediated chloride secretion by human airway epithelial cells, a key driving force for mucociliary clearance. The aim of this study was to investigate the mechanism whereby Cif reduces CFTR-mediated chloride secretion. Cif redirected endocytosed CFTR from recycling endosomes to lysosomes by stabilizing an inhibitory effect of G3BP1 on the deubiquitinating enzyme (DUB), USP10, thereby reducing USP10-mediated deubiquitination of CFTR and increasing the degradation of CFTR in lysosomes. This is the first example of a bacterial toxin that regulates the activity of a host DUB. These data suggest that the ability of P. aeruginosa to chronically infect the lungs of patients with COPD, pneumonia, CF, and bronchiectasis is due in part to the secretion of OMV containing Cif, which inhibits CFTR-mediated chloride secretion and thereby reduces the mucociliary clearance of pathogens.
format	article
author	Jennifer M Bomberger Siying Ye Daniel P Maceachran Katja Koeppen Roxanna L Barnaby George A O'Toole Bruce A Stanton
author_facet	Jennifer M Bomberger Siying Ye Daniel P Maceachran Katja Koeppen Roxanna L Barnaby George A O'Toole Bruce A Stanton
author_sort	Jennifer M Bomberger
title	A Pseudomonas aeruginosa toxin that hijacks the host ubiquitin proteolytic system.
title_short	A Pseudomonas aeruginosa toxin that hijacks the host ubiquitin proteolytic system.
title_full	A Pseudomonas aeruginosa toxin that hijacks the host ubiquitin proteolytic system.
title_fullStr	A Pseudomonas aeruginosa toxin that hijacks the host ubiquitin proteolytic system.
title_full_unstemmed	A Pseudomonas aeruginosa toxin that hijacks the host ubiquitin proteolytic system.
title_sort	pseudomonas aeruginosa toxin that hijacks the host ubiquitin proteolytic system.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/056d8f81590b4b6a92ec79bf107cbb57
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A Pseudomonas aeruginosa toxin that hijacks the host ubiquitin proteolytic system.

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