ArticleRespiratory research2021
Loss of IL-33 enhances elastase-induced and cigarette smoke extract-induced emphysema in mice.
Article in Respiratory research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed, 19 citations in OpenAlex.
- Blocking interleukin 33 reduces joint, systemic, and lung inflammatory responses in the combined collagen-induced arthritis-inhalant endotoxin exposure model.The Journal of pharmacology and experimental therapeutics · 2026Article
- PAI-1 Inhibitor TM5441 Attenuates Emphysema and Airway Inflammation in a Murine Model of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2025Article
- SignallingERJ open research · 2025Article
- Therapeutic targeting of full-length interleukin-33 protein levels with cell-permeable decoy peptides attenuates fibrosis in the bleomycin model in vivo.The Journal of pharmacology and experimental therapeutics · 2025Article
- Article
- Apoptosis inhibitor of macrophage (AIM)/CD5L is involved in the pathogenesis of COPD.Respiratory research · 2023Article
- Animal models: An essential tool to dissect the heterogeneity of chronic obstructive pulmonary disease.Journal of translational internal medicine · 2023Article
- IL-33 Deficiency Attenuates Lung Inflammation by Inducing Th17 Response and Impacting the Th17/Treg Balance in LPS-Induced ARDS Mice via Dendritic Cells.Journal of immunology research · 2022Article
- Elastase- and LPS-Exposed Cpa3Frontiers in immunology · 2022Article
- Reactive Oxygen Species and Antioxidative Defense in Chronic Obstructive Pulmonary Disease.Antioxidants (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIL-33, which is known to induce type 2 immune responses via group 2 innate lymphoid cells, has been reported to contribute to neutrophilic airway inflammation in chronic obstructive pulmonary disease. However, its role in the pathogenesis of emphysema remains unclear.
methodsWe determined the role of interleukin (IL)-33 in the development of emphysema using porcine pancreas elastase (PPE) and cigarette smoke extract (CSE) in mice. First, IL-33
resultsIntratracheal instillation of PPE induced emphysematous changes and increased IL-33 levels in the lungs. Compared to WT mice, IL-33
conclusionThese observations suggest that loss of IL-33 promotes the development of emphysema and may be potentially harmful to patients with 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.