ArticleThorax2014
Innate immunity but not NLRP3 inflammasome activation correlates with severity of stable COPD.
Article in Thorax, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
65 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Association between HMGB1 and COPD: A Systematic Review.Mediators of inflammation · 2015Pooled it
- Pyroptosis in chronic obstructive pulmonary disease: Beyond the canonical NLRP3/Caspase-1/GSDMD pathway.Immunologic research · 2026Review
- Lung NR3C1Communications biology · 2025Article
- The expanding role of the NLRP3 inflammasome from periodic fevers to therapeutic targets.Nature immunology · 2025Review
- Impaired SERPIN-Protease Balance in the Peripheral Lungs of Stable COPD Patients.International journal of molecular sciences · 2025Article
- Host Serine Proteases and Antiviral Innate Immunity as Potential Therapeutic Targets in Influenza A Virus Infection-Induced COPD Exacerbations.International journal of molecular sciences · 2025Article
- NLRP3 is a BMI-independent mediator of stable COPD.BMC pulmonary medicine · 2025Article
- Role of ATG4 Autophagy-Related Protein Family in the Lower Airways of Patients with Stable COPD.International journal of molecular sciences · 2024Article
- Molecular Characterization of the Distal Lung: Novel Insights from Chronic Obstructive Pulmonary Disease Omics.American journal of respiratory and critical care medicine · 2024Article
- Article
- Mitochondrial damage-associated molecular patterns in chronic obstructive pulmonary disease: Pathogenetic mechanism and therapeutic target.Journal of translational internal medicine · 2023Article
- Impaired autophagy in the lower airways and lung parenchyma in stable COPD.ERJ open research · 2023Article
- Bone Morphogenic Proteins and Their Antagonists in the Lower Airways of Stable COPD Patients.Biology · 2023Article
- Oxidised IL-33 drives COPD epithelial pathogenesisThe European respiratory journal · 2023Article
- 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
- Targeting interleukin-33 and thymic stromal lymphopoietin pathways for novel pulmonary therapeutics in asthma and COPD.European respiratory review : an official journal of the European Respiratory Society · 2023Review
- The Anti-Inflammatory Effect of Lactose-Modified Hyaluronic Acid Molecules on Primary Bronchial Fibroblasts of Smokers.Polymers · 2023Article
- Decreased humoral immune response in the bronchi of rapid decliners with chronic obstructive pulmonary disease.Respiratory research · 2022Article
- Activation of NLRP3 inflammasome in stable chronic obstructive pulmonary disease.Scientific reports · 2022Article
- Exosomes derived from adipose-derived stem cells alleviate cigarette smoke-induced lung inflammation and injury by inhibiting alveolar macrophages pyroptosis.Respiratory research · 2022Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 7 institutions in 4 countries.
Funding
Abstract
backgroundIn models of COPD, environmental stressors induce innate immune responses, inflammasome activation and inflammation. However, the interaction between these responses and their role in driving pulmonary inflammation in stable COPD is unknown.
objectivesTo investigate the activation of innate immunity and inflammasome pathways in the bronchial mucosa and bronchoalveolar lavage (BAL) of patients with stable COPD of different severity and control healthy smokers and non-smokers.
methodsInnate immune mediators (interleukin (IL)-6, IL-7, IL-10, IL-27, IL-37, thymic stromal lymphopoietin (TSLP), interferon γ and their receptors, STAT1 and pSTAT1) and inflammasome components (NLRP3, NALP7, caspase 1, IL-1β and its receptors, IL-18, IL-33, ST2) were measured in the bronchial mucosa using immunohistochemistry. IL-6, soluble IL-6R, sgp130, IL-7, IL-27, HMGB1, IL-33, IL-37 and soluble ST2 were measured in BAL using ELISA.
resultsIn bronchial biopsies IL-27+ and pSTAT1+ cells are increased in patients with severe COPD compared with control healthy smokers. IL-7+ cells are increased in patients with COPD and control smokers compared with control non-smokers. In severe stable COPD IL-7R+, IL-27R+ and TSLPR+ cells are increased in comparison with both control groups. The NALP3 inflammasome is not activated in patients with stable COPD compared with control subjects. The inflammasome inhibitory molecules NALP7 and IL-37 are increased in patients with COPD compared with control smokers. IL-6 levels are increased in BAL from patients with stable COPD compared with control smokers with normal lung function whereas IL-1β and IL-18 were similar across all groups.
conclusionsIncreased expression of IL-27, IL-37 and NALP7 in the bronchial mucosa may be involved in progression of stable COPD.
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Registered trials
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.