ArticleFrontiers in pharmacology2019
AIM2 Inflammasome Activation Leads to IL-1α and TGF-β Release From Exacerbated Chronic Obstructive Pulmonary Disease-Derived Peripheral Blood Mononuclear Cells.
Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Inflammasomes in respiratory diseases: from disease pathogenesis to drug development and use of multi-omics.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Pyroptosis in chronic obstructive pulmonary disease: Beyond the canonical NLRP3/Caspase-1/GSDMD pathway.Immunologic research · 2026Review
- Loss of cPLA2α function attenuates inflammation and epithelial thickening in a mouse model ofCurrent research in microbial sciences · 2026Article
- Review
- Role of the AIM2 Inflammasome in Cancer: Potential Therapeutic Strategies.Biomedicines · 2025Review
- Deletion of absent in melanoma-2 (AIM2) drives bone marrow adipogenesis and impairs bone microarchitecture.GeroScience · 2025Article
- Conventional Chemotherapy and Inflammation: What Is the Role of the Inflammasome in the Tumor Microenvironment?Biomedicines · 2025Review
- Regulatory Roles of Noncanonical Inflammasomes in Inflammatory Lung Diseases.International journal of molecular sciences · 2024Review
- Article
- Inflammasome signalling pathway in the regulation of inflammation - its involvement in the development and exacerbation of asthma and chronic obstructive pulmonary disease.Postepy dermatologii i alergologii · 2023Review
- Phenotypic Profiling of Immune Cells and Their Mediators in Chronic Obstructive Pulmonary Disease.Biomedicines · 2023Article
- Regulatory Cues in Pulmonary Fibrosis-With Emphasis on the AIM2 Inflammasome.International journal of molecular sciences · 2023Review
- S1P-Induced TNF-α and IL-6 Release from PBMCs Exacerbates Lung Cancer-Associated Inflammation.Cells · 2022Article
- Polyphenols, flavonoids and inflammasomes: the role of cigarette smoke in COPD.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Activation of the AIM2 Receptor in Circulating Cells of Post-COVID-19 Patients With Signs of Lung Fibrosis Is Associated With the Release of IL-1α, IFN-α and TGF-β.Frontiers in immunology · 2022Article
- Activation and Regulation of NLRP3 by Sterile and Infectious Insults.Frontiers in immunology · 2022Review
- Caspase-11 and AIM2 inflammasome are involved in smoking-induced COPD and lung adenocarcinoma.Oncotarget · 2021Article
- AIM2 nuclear exit and inflammasome activation in chronic obstructive pulmonary disease and response to cigarette smoke.Journal of inflammation (London, England) · 2021Article
- Roles of Inflammasome in Cigarette Smoke-Related Diseases and Physiopathological Disorders: Mechanisms and Therapeutic Opportunities.Frontiers in immunology · 2021Review
- Antioxidant and antimicrobial properties of Pelargonium sidoides DC and lactoferrin combination.Bioscience reports · 2020Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic obstructive pulmonary disease (COPD) is now the fourth-leading cause of death worldwide and its prevalence is increasing. The progressive decline of lung function and airway remodelling are a consequence of chronic inflammatory responses. It was recently postulated the involvement of the inflammasome in COPD, although the underlying mechanism/s still need to be elucidated. Therefore, we isolated peripheral blood mononuclear cells (PBMCs) from exacerbated/unstable COPD patients. The stimulation of PBMCs with an AIM2 inflammasome activator, Poly dA:dT, led to IL-1α, but not IL-1β, release. The release of this cytokine was caspase-1- and caspase-4-dependent and correlated to higher levels of 8-OH-dG in COPD compared to non-smoker and smoker-derived PBMCs. Interestingly, AIM2-depedent IL-1α release was responsible for higher TGF-β levels, crucial mediator during pro-fibrotic processes associated to COPD progression. In conclusion, our data highlight the involvement of AIM2/caspase-1/caspase-4 in IL-1α-induced TGF-β release in unstable COPD-derived PBMCs, opening new therapeutic perspectives for unstable COPD patients.
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