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...
Main Authors: | , , , , , , , , |
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Format: | Article |
Language: | English |
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Frontiers Media S.A.
2016-11-01
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Series: | Frontiers in Cellular and Infection Microbiology |
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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. |
first_indexed | 2024-12-11T17:46:12Z |
format | Article |
id | doaj.art-17b78e50d0d24f51ab3a6268dad4e019 |
institution | Directory Open Access Journal |
issn | 2235-2988 |
language | English |
last_indexed | 2024-12-11T17:46:12Z |
publishDate | 2016-11-01 |
publisher | Frontiers Media S.A. |
record_format | Article |
series | Frontiers in Cellular and Infection Microbiology |
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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