ArticleFrontiers in immunology2021
Enhanced IL-1β Release Following NLRP3 and AIM2 Inflammasome Stimulation Is Linked to mtROS in Airway Macrophages in Pulmonary Fibrosis.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 75 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
- ERS Congress 2025: highlights from the Paediatrics Assembly.ERJ open research · 2026Review
- Mitochondria Meet the Lung Microbiome: A Bidirectional Dialogue in Inflammation and Respiratory Diseases.Biomedicines · 2026Review
- Immunoregulatory mechanisms in parasitic eosinophilic lung disease: the role of IgE immune complexes and NLRC4 inflammasome.Frontiers in immunology · 2026Review
- The mitochondrial logic of inflammaging: how energy imbalance drives fibroblast SASP and tissue-specific aging.Frontiers in immunology · 2026Review
- Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies.Frontiers in immunology · 2026Review
- Microbiome-innate immune crosstalk in acute exacerbation of idiopathic pulmonary fibrosis: an amplification framework.Frontiers in immunology · 2026Review
- Nanotechnology-based targeted regulation of NLRP3 Inflammasome: therapeutic strategies and clinical application prospects in inflammatory diseases.Drug delivery · 2025Review
- Altered Metabolism in Idiopathic Pulmonary Fibrosis.Journal of cellular physiology · 2025Review
- Precision-Cut Liver Slices: A Valuable Preclinical Tool for Translational Research in Liver Fibrosis.International journal of molecular sciences · 2025Article
- Insights into interstitial lung disease pathogenesis.Breathe (Sheffield, England) · 2025Review
- Resveratrol-Enhanced Human Neural Stem Cell-Derived Exosomes Mitigate MPP+-Induced Neurotoxicity Through Activation of AMPK and Nrf2 Pathways and Inhibition of the NLRP3 Inflammasome in SH-SY5Y Cells.Life (Basel, Switzerland) · 2025Article
- MAM-STAT3-Driven Mitochondrial CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Macrophage pyroptosis mediates hyperoxia-induced inflammatory lung injury in neonates.Frontiers in immunology · 2025Article
- Feasibility of Absent in Melanoma 2 as a Serological Marker in Relation to Complicated Community-Acquired Pneumonia in Children: A Prospective Cohort Study.International journal of general medicine · 2025Article
- The role of antibiotic-derived mycobacterial vesicles in tuberculosis pathogenesis.Scientific reports · 2024Article
- Opposite effects of systemic and local conditional CD11c+ myeloid cell depletion during bleomycin-induced inflammation and fibrosis in mice.Immunity, inflammation and disease · 2024Article
- Biomaterial Fg/P(LLA-CL) regulates macrophage polarization and recruitment of mesenchymal stem cells after endometrial injury.Journal of materials science. Materials in medicine · 2024Article
- Lactate facilitated mitochondrial fission-derived ROS to promote pulmonary fibrosis via ERK/DRP-1 signaling.Journal of translational medicine · 2024Article
- Vinpocetine alleviated alveolar epithelial cells injury in experimental pulmonary fibrosis by targeting PPAR-γ/NLRP3/NF-κB and TGF-β1/Smad2/3 pathways.Scientific reports · 2024Article
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
Fibrotic Interstitial lung diseases (ILDs) are complex disorders of variable clinical behaviour. The majority of them cause significant morbidity, whilst Idiopathic Pulmonary Fibrosis (IPF) is recognised as the most relentless. NLRP3, AIM2, and NLRC4 inflammasomes are multiprotein complexes driving IL-1β release; a proinflammatory and profibrotic cytokine. Several pathogenetic factors associated with IPF are identified as inflammasome activators, including increases in mtROS and bacterial burden. Mitochondrial oxidation and alterations in bacterial burden in IPF and other ILDs may lead to augmented inflammasome activity in airway macrophages (AMs). IPF (n=14), non-IPF-ILDs (n=12) patients and healthy subjects (n=12) were prospectively recruited and AMs were isolated from bronchoalveolar lavage. IL-1β release resulting from NLRP3, AIM2 and NLRC4 inflammasomes stimulation in AMs were determined and baseline levels of mitochondrial ROS and microbial burden were also measured. Our results showed that NLRP3 was more inducible in IPF and other ILDs compared to controls. Additionally, following AIM2 activation IL-1β release was significantly higher in IPF compared to controls, whereas similar trends were observed in Non-IPF-ILDs. NLRC4 activation was similar across groups. mtROS was significantly associated with heightened NLRP3 and AIM2 activation, and mitochondrial antioxidant treatment limited inflammasome activation. Importantly, microbial burden was linked to baseline IL-1β release and
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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.