ArticleFrontiers in immunology2018
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.
Article in Frontiers in immunology, 2018. 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, 31 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
- Role of the AIM2 Inflammasome in Cancer: Potential Therapeutic Strategies.Biomedicines · 2025Review
- Absent in melanoma 2: a potent suppressor of retinal pigment epithelial-mesenchymal transition and experimental proliferative vitreoretinopathy.Cell death & disease · 2025Article
- Regulatory Roles of Noncanonical Inflammasomes in Inflammatory Lung Diseases.International journal of molecular sciences · 2024Review
- PANoptosis: Mechanism and Role in Pulmonary Diseases.International journal of molecular sciences · 2023Review
- Niclosamide Attenuates Inflammation-Associated Profibrotic Responses in Human Subepithelial Lung Myofibroblasts.Biomedicines · 2023Article
- Regulatory Cues in Pulmonary Fibrosis-With Emphasis on the AIM2 Inflammasome.International journal of molecular sciences · 2023Review
- Cytoplasmic DNAs: Sources, sensing, and roles in the development of lung inflammatory diseases and cancer.Frontiers in immunology · 2023Review
- Common Molecular Pathways Between Post-COVID19 Syndrome and Lung Fibrosis: A Scoping Review.Frontiers in pharmacology · 2022Article
- Role of Pyroptosis in Respiratory Diseases and its Therapeutic Potential.Journal of inflammation research · 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
- Examination of the role of necroptotic damage-associated molecular patterns in tissue fibrosis.Frontiers in immunology · 2022Review
- Post-COVID-19 Patients Who Develop Lung Fibrotic-like Changes Have Lower Circulating Levels of IFN-β but Higher Levels of IL-1α and TGF-β.Biomedicines · 2021Article
- Article
- Caspase-11 and AIM2 inflammasome are involved in smoking-induced COPD and lung adenocarcinoma.Oncotarget · 2021Article
- Enhanced IL-1β Release Following NLRP3 and AIM2 Inflammasome Stimulation Is Linked to mtROS in Airway Macrophages in Pulmonary Fibrosis.Frontiers in immunology · 2021Article
- Inflammasomes and Fibrosis.Frontiers in immunology · 2021Review
- Antioxidant and antimicrobial properties of Pelargonium sidoides DC and lactoferrin combination.Bioscience reports · 2020Article
- Identification of a novel subpopulation of Caspase-4 positive non-small cell lung Cancer patients.Journal of experimental & clinical cancer research : CR · 2020Article
- DROSHA-Dependent miRNA and AIM2 Inflammasome Activation in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic fibro-proliferative disease characterized by poor prognosis, with a mean survival of ~2-3 years after definite diagnosis. The cause of IPF is still unknown but it is a heterogeneous condition in which the aberrant deposition of extracellular matrix leads to extensive lung remodeling. This remodeling is a consequence of inflammatory responses, but the mechanisms involved are poorly understood. In this study, we first analyzed a bleomycin-induced mouse model, which showed that higher expression of IL-1β, but not IL-18, was correlated to pulmonary cell infiltration and fibrosis. Then, we found that peripheral blood mononuclear cells (PBMCs) from IPF patients released IL-1α and IL-18 in a NLRP3- and calpain-independent manner after LPS ± ATP stimulation. Instead, the activation of the absent in melanoma 2 (AIM2) inflammasome induced the release of IL-1α in a caspase-1-/caspase-8-independent manner; whereas IL-18 release was caspase-1 dependent. These effects correlated with the release of the pro-fibrotic TGF-β, which was induced by AIM2 activation in a caspase-1- and TLR4-independent manner, but dependent on IL-1α. In this context, the activation of AIM2 induced the release of caspase-4 from IPF-derived PBMCs, which correlated with the mRNA levels of this caspase that was higher in IPF than in healthy PBMCs. In conclusion, our findings identify a novel molecular mechanism whereby the activation of AIM2 could lead to the activation of the non-canonical inflammasome (caspase-4 dependent) that induces the release of IL-1α responsible for the release of TGF-β from PBMCs of IPF patients.
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