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Chronic Obstructive Pulmonary Disease-Derived Circulating Cells Release IL-18 and IL-33 under Ultrafine Particulate Matter Exposure in a Caspase-1/8-Independent Manner

Chronic obstructive pulmonary disease (COPD) is considered the fourth-leading causes of death worldwide; COPD is caused by inhalation of noxious indoor and outdoor particles, especially cigarette smoke that represents the first risk factor for this respiratory disorder. To mimic the effects of parti...

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Autores principales: De Falco, Gianluigi, Colarusso, Chiara, Terlizzi, Michela, Popolo, Ada, Pecoraro, Michela, Commodo, Mario, Minutolo, Patrizia, Sirignano, Mariano, D’Anna, Andrea, Aquino, Rita P., Pinto, Aldo, Molino, Antonio, Sorrentino, Rosalinda
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5662642/
https://www.ncbi.nlm.nih.gov/pubmed/29123531
http://dx.doi.org/10.3389/fimmu.2017.01415
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author De Falco, Gianluigi
Colarusso, Chiara
Terlizzi, Michela
Popolo, Ada
Pecoraro, Michela
Commodo, Mario
Minutolo, Patrizia
Sirignano, Mariano
D’Anna, Andrea
Aquino, Rita P.
Pinto, Aldo
Molino, Antonio
Sorrentino, Rosalinda
author_facet De Falco, Gianluigi
Colarusso, Chiara
Terlizzi, Michela
Popolo, Ada
Pecoraro, Michela
Commodo, Mario
Minutolo, Patrizia
Sirignano, Mariano
D’Anna, Andrea
Aquino, Rita P.
Pinto, Aldo
Molino, Antonio
Sorrentino, Rosalinda
author_sort De Falco, Gianluigi
collection PubMed
description Chronic obstructive pulmonary disease (COPD) is considered the fourth-leading causes of death worldwide; COPD is caused by inhalation of noxious indoor and outdoor particles, especially cigarette smoke that represents the first risk factor for this respiratory disorder. To mimic the effects of particulate matter on COPD, we isolated peripheral blood mononuclear cells (PBMCs) and treated them with combustion-generated ultrafine particles (UFPs) obtained from two different fuel mixtures, namely, pure ethylene and a mixture of ethylene and dimethylfuran (the latter mimicking the combustion of biofuels). UFPs were separated in two fractions: (1) sub-10 nm particles, named nano organic carbon (NOC) particles and (2) primarily soot particles of 20–40 nm and their agglomerates (200 nm). We found that both NOC and soot UFPs induced the release of IL-18 and IL-33 from unstable/exacerbated COPD-derived PBMCs. This effect was associated with higher levels of mitochondrial dysfunction and derived reactive oxygen species, which were higher in PBMCs from unstable COPD patients after combustion-generated UFP exposure. Moreover, lower mRNA expression of the repairing enzyme OGG1 was associated with the higher levels of 8-OH-dG compared with non-smoker and smokers. It was interesting that IL-18 and IL-33 release from PBMCs of unstable COPD patients was not NOD-like receptor 3/caspase-1 or caspase-8-dependent, but rather correlated to caspase-4 release. This effect was not evident in stable COPD-derived PBMCs. Our data suggest that combustion-generated UFPs induce the release of caspase-4-dependent inflammasome from PBMCs of COPD patients compared with healthy subjects, shedding new light into the biology of this key complex in COPD.
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spelling pubmed-56626422017-11-09 Chronic Obstructive Pulmonary Disease-Derived Circulating Cells Release IL-18 and IL-33 under Ultrafine Particulate Matter Exposure in a Caspase-1/8-Independent Manner De Falco, Gianluigi Colarusso, Chiara Terlizzi, Michela Popolo, Ada Pecoraro, Michela Commodo, Mario Minutolo, Patrizia Sirignano, Mariano D’Anna, Andrea Aquino, Rita P. Pinto, Aldo Molino, Antonio Sorrentino, Rosalinda Front Immunol Immunology Chronic obstructive pulmonary disease (COPD) is considered the fourth-leading causes of death worldwide; COPD is caused by inhalation of noxious indoor and outdoor particles, especially cigarette smoke that represents the first risk factor for this respiratory disorder. To mimic the effects of particulate matter on COPD, we isolated peripheral blood mononuclear cells (PBMCs) and treated them with combustion-generated ultrafine particles (UFPs) obtained from two different fuel mixtures, namely, pure ethylene and a mixture of ethylene and dimethylfuran (the latter mimicking the combustion of biofuels). UFPs were separated in two fractions: (1) sub-10 nm particles, named nano organic carbon (NOC) particles and (2) primarily soot particles of 20–40 nm and their agglomerates (200 nm). We found that both NOC and soot UFPs induced the release of IL-18 and IL-33 from unstable/exacerbated COPD-derived PBMCs. This effect was associated with higher levels of mitochondrial dysfunction and derived reactive oxygen species, which were higher in PBMCs from unstable COPD patients after combustion-generated UFP exposure. Moreover, lower mRNA expression of the repairing enzyme OGG1 was associated with the higher levels of 8-OH-dG compared with non-smoker and smokers. It was interesting that IL-18 and IL-33 release from PBMCs of unstable COPD patients was not NOD-like receptor 3/caspase-1 or caspase-8-dependent, but rather correlated to caspase-4 release. This effect was not evident in stable COPD-derived PBMCs. Our data suggest that combustion-generated UFPs induce the release of caspase-4-dependent inflammasome from PBMCs of COPD patients compared with healthy subjects, shedding new light into the biology of this key complex in COPD. Frontiers Media S.A. 2017-10-26 /pmc/articles/PMC5662642/ /pubmed/29123531 http://dx.doi.org/10.3389/fimmu.2017.01415 Text en Copyright © 2017 De Falco, Colarusso, Terlizzi, Popolo, Pecoraro, Commodo, Minutolo, Sirignano, D’Anna, Aquino, Pinto, Molino and Sorrentino. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
De Falco, Gianluigi
Colarusso, Chiara
Terlizzi, Michela
Popolo, Ada
Pecoraro, Michela
Commodo, Mario
Minutolo, Patrizia
Sirignano, Mariano
D’Anna, Andrea
Aquino, Rita P.
Pinto, Aldo
Molino, Antonio
Sorrentino, Rosalinda
Chronic Obstructive Pulmonary Disease-Derived Circulating Cells Release IL-18 and IL-33 under Ultrafine Particulate Matter Exposure in a Caspase-1/8-Independent Manner
title Chronic Obstructive Pulmonary Disease-Derived Circulating Cells Release IL-18 and IL-33 under Ultrafine Particulate Matter Exposure in a Caspase-1/8-Independent Manner
title_full Chronic Obstructive Pulmonary Disease-Derived Circulating Cells Release IL-18 and IL-33 under Ultrafine Particulate Matter Exposure in a Caspase-1/8-Independent Manner
title_fullStr Chronic Obstructive Pulmonary Disease-Derived Circulating Cells Release IL-18 and IL-33 under Ultrafine Particulate Matter Exposure in a Caspase-1/8-Independent Manner
title_full_unstemmed Chronic Obstructive Pulmonary Disease-Derived Circulating Cells Release IL-18 and IL-33 under Ultrafine Particulate Matter Exposure in a Caspase-1/8-Independent Manner
title_short Chronic Obstructive Pulmonary Disease-Derived Circulating Cells Release IL-18 and IL-33 under Ultrafine Particulate Matter Exposure in a Caspase-1/8-Independent Manner
title_sort chronic obstructive pulmonary disease-derived circulating cells release il-18 and il-33 under ultrafine particulate matter exposure in a caspase-1/8-independent manner
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5662642/
https://www.ncbi.nlm.nih.gov/pubmed/29123531
http://dx.doi.org/10.3389/fimmu.2017.01415
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