ArticleScientific reports2017
Human peripheral blood mononuclear cells (PBMCs) from smokers release higher levels of IL-1-like cytokines after exposure to combustion-generated ultrafine particles.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Peripheral blood mononuclear cell mitochondrial bioenergetics are related to vascular endothelial function in young and older adults.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Article
- Fine particulate matter aggravates smoking induced lung injury via NLRP3/caspase-1 pathway in COPD.Journal of inflammation (London, England) · 2024Article
- Contribution of adaptive immunity to human COPD and experimental models of emphysema.Physiological reviews · 2023Review
- Article
- The Paradigm Change of IL-33 in Vascular Biology.International journal of molecular sciences · 2021Review
- Caspase-11 and AIM2 inflammasome are involved in smoking-induced COPD and lung adenocarcinoma.Oncotarget · 2021Article
- NKp30 - A prospective target for new cancer immunotherapy strategies.British journal of pharmacology · 2020Review
- New Insights into the Implication of Mitochondrial Dysfunction in Tissue, Peripheral Blood Mononuclear Cells, and Platelets during Lung Diseases.Journal of clinical medicine · 2020Review
- DROSHA-Dependent miRNA and AIM2 Inflammasome Activation in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2020Review
- Proinflammatory effects of dust storm and thermal inversion particulate matter (PMJournal of environmental health science & engineering · 2019Article
- The Inhibition of Caspase-1- Does Not Revert Particulate Matter (PM)-Induced Lung Immunesuppression in Mice.Frontiers in immunology · 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
- 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
- Circulating and tumor-associated caspase-4: a novel diagnostic and prognostic biomarker for non-small cell lung cancer.Oncotarget · 2018Article
- Activation of the Absent in Melanoma 2 Inflammasome in Peripheral Blood Mononuclear Cells From Idiopathic Pulmonary Fibrosis Patients Leads to the Release of Pro-Fibrotic Mediators.Frontiers in immunology · 2018Article
- Article
- 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 · 2017Article
- Tobacco use and neurogenesis: A theoretical review of pathophysiological mechanism affecting the outcome of peripheral nerve regeneration.Journal of orthopaedicsReview
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ultrafine particles (UFP) generated by combustion processes are often associated with adverse health effects. However, little is known about the inflammatory processes generated by UFP that may underlie their toxicological activity. Murine macrophages (J774.1 cells) and human peripheral blood mononuclear cells (PBMCs) were used to evaluate the molecular mechanism underlying the pro-inflammatory activity of UFP. The addition of soot particles to J774.1 cells induced a concentration-dependent release of IL-1α, IL-1β and IL-33 This effect was not associated with cell death and, in contrast to literature, was pronounced at very low concentrations (5-100 pg/ml). Similarly, UFP induced the release of IL-1α, IL-18 and IL-33 by PBMCs. However, this effect was solely observed in PBMCs obtained from smokers, as the PBMCs from non-smokers instead released higher levels of IL-10. The release of these cytokines after UFP exposure was caspase-1- and NLRP3 inflammasome-dependent in PBMCs from healthy smokers, whereas IL-1α release was calpain-dependent. These results show that UFP at very low concentrations are able to give rise to an inflammatory process that is responsible for IL-1α, IL-18 and IL-33 release, which is pronounced in PBMCs from smokers, confirming that these individuals are especially susceptible to inflammatory-based airway diseases once exposed to air pollution.
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