Pseudomonas aeruginosa airway infection recruits and modulates neutrophilic myeloid-derived suppressor cells

Pseudomonas aeruginosa is an opportunistic pathogen that causes infections mainly in patients with cystic fibrosis (CF) lung disease. Despite innate and adaptive immune responses upon infection, P. aeruginosa is capable of efficiently escaping host defenses, but the underlying immune mechanisms rema...

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Main Authors: Hasan Halit Öz, Benyuan Zhou, Pina Voss, Melanie Carevic, Carolin Schroth, Nina Frey, Nikolaus Rieber, Andreas Hector, Dominik Hartl
Format: Article
Language:English
Published: Frontiers Media S.A. 2016-11-01
Series:Frontiers in Cellular and Infection Microbiology
Subjects:
Online Access:http://journal.frontiersin.org/Journal/10.3389/fcimb.2016.00167/full
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author Hasan Halit Öz
Benyuan Zhou
Pina Voss
Melanie Carevic
Carolin Schroth
Nina Frey
Nikolaus Rieber
Nikolaus Rieber
Andreas Hector
Dominik Hartl
Dominik Hartl
author_facet Hasan Halit Öz
Benyuan Zhou
Pina Voss
Melanie Carevic
Carolin Schroth
Nina Frey
Nikolaus Rieber
Nikolaus Rieber
Andreas Hector
Dominik Hartl
Dominik Hartl
author_sort Hasan Halit Öz
collection DOAJ
description Pseudomonas aeruginosa is an opportunistic pathogen that causes infections mainly in patients with cystic fibrosis (CF) lung disease. Despite innate and adaptive immune responses upon infection, P. aeruginosa is capable of efficiently escaping host defenses, but the underlying immune mechanisms remain poorly understood. Myeloid-derived suppressor cells (MDSCs) are innate immune cells that are functionally characterized by their potential to suppress T- and natural killer (NK)-cell responses. Here we demonstrate, using an airway in vivo infection model, that P. aeruginosa recruits and activates neutrophilic MDSCs, which functionally suppress T-cell responses. We further show that the CF gene defect (cystic fibrosis transmembrane conductance regulator, CFTR) modulates the functionality, but not the recruitment or generation of neutrophilic MDSCs. Collectively, we define a mechanism by which P. aeruginosa airway infection undermines host immunity by modulating neutrophilic MDSCs in vivo.
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spelling doaj.art-17b78e50d0d24f51ab3a6268dad4e0192022-12-22T00:56:21ZengFrontiers Media S.A.Frontiers in Cellular and Infection Microbiology2235-29882016-11-01610.3389/fcimb.2016.00167221686Pseudomonas aeruginosa airway infection recruits and modulates neutrophilic myeloid-derived suppressor cellsHasan Halit Öz0Benyuan Zhou1Pina Voss2Melanie Carevic3Carolin Schroth4Nina Frey5Nikolaus Rieber6Nikolaus Rieber7Andreas Hector8Dominik Hartl9Dominik Hartl10University of TübingenUniversity of TübingenUniversity of TübingenUniversity of TübingenUniversity of TübingenUniversity of TübingenTechnische Universität MünchenUniversity of TübingenUniversity of TübingenRoche Pharma Research & Early DevelopmentUniversity of TübingenPseudomonas aeruginosa is an opportunistic pathogen that causes infections mainly in patients with cystic fibrosis (CF) lung disease. Despite innate and adaptive immune responses upon infection, P. aeruginosa is capable of efficiently escaping host defenses, but the underlying immune mechanisms remain poorly understood. Myeloid-derived suppressor cells (MDSCs) are innate immune cells that are functionally characterized by their potential to suppress T- and natural killer (NK)-cell responses. Here we demonstrate, using an airway in vivo infection model, that P. aeruginosa recruits and activates neutrophilic MDSCs, which functionally suppress T-cell responses. We further show that the CF gene defect (cystic fibrosis transmembrane conductance regulator, CFTR) modulates the functionality, but not the recruitment or generation of neutrophilic MDSCs. Collectively, we define a mechanism by which P. aeruginosa airway infection undermines host immunity by modulating neutrophilic MDSCs in vivo.http://journal.frontiersin.org/Journal/10.3389/fcimb.2016.00167/fullCystic FibrosisLungPseudomonas aeruginosaT cellsCFTRmyeloid-derived suppressor cells
spellingShingle Hasan Halit Öz
Benyuan Zhou
Pina Voss
Melanie Carevic
Carolin Schroth
Nina Frey
Nikolaus Rieber
Nikolaus Rieber
Andreas Hector
Dominik Hartl
Dominik Hartl
Pseudomonas aeruginosa airway infection recruits and modulates neutrophilic myeloid-derived suppressor cells
Frontiers in Cellular and Infection Microbiology
Cystic Fibrosis
Lung
Pseudomonas aeruginosa
T cells
CFTR
myeloid-derived suppressor cells
title Pseudomonas aeruginosa airway infection recruits and modulates neutrophilic myeloid-derived suppressor cells
title_full Pseudomonas aeruginosa airway infection recruits and modulates neutrophilic myeloid-derived suppressor cells
title_fullStr Pseudomonas aeruginosa airway infection recruits and modulates neutrophilic myeloid-derived suppressor cells
title_full_unstemmed Pseudomonas aeruginosa airway infection recruits and modulates neutrophilic myeloid-derived suppressor cells
title_short Pseudomonas aeruginosa airway infection recruits and modulates neutrophilic myeloid-derived suppressor cells
title_sort pseudomonas aeruginosa airway infection recruits and modulates neutrophilic myeloid derived suppressor cells
topic Cystic Fibrosis
Lung
Pseudomonas aeruginosa
T cells
CFTR
myeloid-derived suppressor cells
url http://journal.frontiersin.org/Journal/10.3389/fcimb.2016.00167/full
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