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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.
Front Immunol 2017; 8:1415FI

Abstract

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.

Authors+Show Affiliations

Dipartimento di Ingegneria Chimica, dei Materiali e della Produzione Industriale, Università degli Studi di Napoli Federico II, Naples, Italy.Department of Pharmacy, University of Salerno, Fisciano, Italy. ImmunePharma s.r.l., University of Salerno, Fisciano, Italy. Drug Discovery and Development Program, Department of Pharmacy, University of Salerno, Fisciano, Italy.Department of Pharmacy, University of Salerno, Fisciano, Italy. ImmunePharma s.r.l., University of Salerno, Fisciano, Italy.Department of Pharmacy, University of Salerno, Fisciano, Italy. ImmunePharma s.r.l., University of Salerno, Fisciano, Italy.Department of Pharmacy, University of Salerno, Fisciano, Italy. ImmunePharma s.r.l., University of Salerno, Fisciano, Italy.Institute for Research on Combustion (CNR), Naples, Italy.Institute for Research on Combustion (CNR), Naples, Italy.Dipartimento di Ingegneria Chimica, dei Materiali e della Produzione Industriale, Università degli Studi di Napoli Federico II, Naples, Italy.Dipartimento di Ingegneria Chimica, dei Materiali e della Produzione Industriale, Università degli Studi di Napoli Federico II, Naples, Italy.Department of Pharmacy, University of Salerno, Fisciano, Italy. ImmunePharma s.r.l., University of Salerno, Fisciano, Italy.Department of Pharmacy, University of Salerno, Fisciano, Italy. ImmunePharma s.r.l., University of Salerno, Fisciano, Italy.Department of Respiratory Medicine, Respiratory Division, University of Naples Federico II, Naples, Italy.Department of Pharmacy, University of Salerno, Fisciano, Italy. ImmunePharma s.r.l., University of Salerno, Fisciano, Italy.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29123531

Citation

De Falco, Gianluigi, et al. "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." Frontiers in Immunology, vol. 8, 2017, p. 1415.
De Falco G, Colarusso C, Terlizzi M, et al. 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. Front Immunol. 2017;8:1415.
De Falco, G., Colarusso, C., Terlizzi, M., Popolo, A., Pecoraro, M., Commodo, M., ... Sorrentino, R. (2017). 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. Frontiers in Immunology, 8, p. 1415. doi:10.3389/fimmu.2017.01415.
De Falco G, et al. 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. Front Immunol. 2017;8:1415. PubMed PMID: 29123531.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - De Falco,Gianluigi, AU - Colarusso,Chiara, AU - Terlizzi,Michela, AU - Popolo,Ada, AU - Pecoraro,Michela, AU - Commodo,Mario, AU - Minutolo,Patrizia, AU - Sirignano,Mariano, AU - D'Anna,Andrea, AU - Aquino,Rita P, AU - Pinto,Aldo, AU - Molino,Antonio, AU - Sorrentino,Rosalinda, Y1 - 2017/10/26/ PY - 2017/08/07/received PY - 2017/10/12/accepted PY - 2017/11/11/entrez PY - 2017/11/11/pubmed PY - 2017/11/11/medline KW - airway disease KW - chronic obstructive pulmonary disease KW - combustion-generated ultrafine particles KW - inflammation KW - peripheral blood mononuclear cells SP - 1415 EP - 1415 JF - Frontiers in immunology JO - Front Immunol VL - 8 N2 - 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. SN - 1664-3224 UR - https://www.unboundmedicine.com/medline/citation/29123531/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_ L2 - https://dx.doi.org/10.3389/fimmu.2017.01415 DB - PRIME DP - Unbound Medicine ER -