ArticleFrontiers in immunology2017
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.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 45 citations in OpenAlex.
- Molecular Duality of OGG1: From Genomic Guardian to Redox-Sensitive Modulator in Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Assessment of NLRP3 inflammasome activation in patients with chronic obstructive pulmonary disease before and after lung transplantation.Immunologic research · 2024Article
- Fine particulate matter aggravates smoking induced lung injury via NLRP3/caspase-1 pathway in COPD.Journal of inflammation (London, England) · 2024Article
- The Role of IL-33/ST2 in COPD and Its Future as an Antibody Therapy.International journal of molecular sciences · 2023Review
- Polyphenols, flavonoids and inflammasomes: the role of cigarette smoke in COPD.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Review
- TI: NLRP3 Inflammasome-Dependent Pyroptosis in CNS Trauma: A Potential Therapeutic Target.Frontiers in cell and developmental biology · 2022Review
- Pyroptosis and respiratory diseases: A review of current knowledge.Frontiers in immunology · 2022Review
- From Biomarkers to Novel Therapeutic Approaches in Chronic Obstructive Pulmonary Disease.Biomedicines · 2021Review
- Caspase-11 and AIM2 inflammasome are involved in smoking-induced COPD and lung adenocarcinoma.Oncotarget · 2021Article
- Interleukin-33 gene polymorphisms and chronic obstructive pulmonary disease in the Chinese Han population.The Journal of international medical research · 2020Article
- Antioxidant and antimicrobial properties of Pelargonium sidoides DC and lactoferrin combination.Bioscience reports · 2020Article
- New Insights into the Implication of Mitochondrial Dysfunction in Tissue, Peripheral Blood Mononuclear Cells, and Platelets during Lung Diseases.Journal of clinical medicine · 2020Review
- IL-33 in Chronic Respiratory Disease: From Preclinical to Clinical Studies.ACS pharmacology & translational science · 2020Review
- Variations in Reactive Oxygen Species Generation by Urban Airborne Particulate Matter in Lung Epithelial Cells-Impact of Inorganic Fraction.Frontiers in chemistry · 2020Article
- Short-term Haze Exposure Predisposes Healthy Volunteers to Nasal Inflammation.Allergy, asthma & immunology research · 2019Article
- AIM2 Inflammasome Activation Leads to IL-1α and TGF-β Release From Exacerbated Chronic Obstructive Pulmonary Disease-Derived Peripheral Blood Mononuclear Cells.Frontiers in pharmacology · 2019Article
- AIM2/IL-1α/TGF-β Axis in PBMCs From Exacerbated Chronic Obstructive Pulmonary Disease (COPD) Patients Is Not Related to COX-2-Dependent Inflammatory Pathway.Frontiers in physiology · 2019Article
- The Inhibition of Caspase-1- Does Not Revert Particulate Matter (PM)-Induced Lung Immunesuppression in Mice.Frontiers in immunology · 2019Article
- Circulating and tumor-associated caspase-4: a novel diagnostic and prognostic biomarker for non-small cell lung cancer.Oncotarget · 2018Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.