ArticleImmunology2013
Anti-interleukin-33 inhibits cigarette smoke-induced lung inflammation in mice.
Article in Immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.
What it found
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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
34 citing papers in PubMed, 70 citations in OpenAlex.
- Distribution of blood eosinophil counts in the Chinese general population.The European respiratory journal · 2026Article
- Association of polymorphisms of antioxidants (GSTM1/T1) and inflammation-related genes (CXCL8, IL-33, and IL-6) with chronic obstructive pulmonary disease (COPD).Journal of applied genetics · 2025Article
- The production, function, and clinical applications of IL-33 in type 2 inflammation-related respiratory diseases.Frontiers in immunology · 2024Review
- A deep insight into ferroptosis in lung disease: facts and perspectives.Frontiers in oncology · 2024Review
- IL-33 Expression Is Lower in Current Smokers at both Transcriptomic and Protein Levels.American journal of respiratory and critical care medicine · 2023Article
- A CpG-Oligodeoxynucleotide Suppresses Th2/Th17 Inflammation by Inhibiting IL-33/ST2 Signaling in Mice from a Model of Adoptive Dendritic Cell Transfer of Smoke-Induced Asthma.International journal of molecular sciences · 2023Article
- Targeting ferroptosis as a vulnerability in pulmonary diseases.Cell death & disease · 2022Review
- Elastase- and LPS-Exposed Cpa3Frontiers in immunology · 2022Article
- Soluble ST2 and All-Cause Mortality in Patients with Chronic Obstructive Pulmonary Disease-A 10-Year Cohort Study.Journal of clinical medicine · 2021Article
- Review
- Loss of IL-33 enhances elastase-induced and cigarette smoke extract-induced emphysema in mice.Respiratory research · 2021Article
- Role of Type2 Inflammatory Biomarkers in Chronic Obstructive Pulmonary Disease.Journal of clinical medicine · 2020Review
- IL-33 promotes type 1 cytokine expression via p38 MAPK in human NK cells.Journal of leukocyte biology · 2020Article
- Blocking Interleukin-33 Alleviates the Joint Inflammation and Inhibits the Development of Collagen-Induced Arthritis in Mice.Journal of immunology research · 2020Article
- Blockade of IL-33 signalling attenuates osteoarthritis.Clinical & translational immunology · 2020Article
- Linking VEGF Deficiency and IL-33 Upregulation in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2019Article
- microRNA-520c-3p suppresses NLRP3 inflammasome activation and inflammatory cascade in preeclampsia by downregulating NLRP3.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Article
- Tobacco smoke induced hepatic cancer stem cell-like properties through IL-33/p38 pathway.Journal of experimental & clinical cancer research : CR · 2019Article
- IL-33 Mediated Inflammation in Chronic Respiratory Diseases-Understanding the Role of the Member of IL-1 Superfamily.Frontiers in immunology · 2019Review
- Leukocyte trafficking between stromal compartments: lessons from rheumatoid arthritis.Nature reviews. Rheumatology · 2018Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The mechanism by which cigarette smoke (CS) causes chronic obstructive pulmonary disease (COPD) is poorly understood. Interleukin-33 (IL-33) is a pleiotropic cytokine predominantly expressed in lung tissue and can elicit airway inflammation in naive mice. We tested the hypothesis that IL-33 is induced by CS and contributes to CS-mediated airway inflammation in a mouse model of CS-induced COPD. Groups of mice were exposed to CS three times per day for 4 consecutive days. The expression levels of IL-33 and ST2 were markedly enhanced in the lung tissue of mice inhaling CS. Exposure to CS also induced neutrophil and macrophage infiltration and expression of inflammatory cytokines (IL-1β, tumour necrosis factor-α, IL-17), chemokines (monocyte chemoattractant protein-1) and mucin 5, subtypes A and C in the airways. More importantly, all of these CS-induced pathogenic changes were significantly inhibited by treatment with neutralizing anti-IL-33 antibody delivered intranasally. Hence, our results suggest that IL-33 plays a critical role in CS-mediated airway inflammation and may be a therapeutic target in CS-related diseases, including 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.