ArticleImmunology2013
Interleukin-33 and alveolar macrophages contribute to the mechanisms underlying the exacerbation of IgE-mediated airway inflammation and remodelling in mice.
Article in Immunology, 2013. 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, 67 citations in OpenAlex.
- Recurrence of acute allergic asthma depends on the role of ILC2 driven by Il1rl1 signaling.Cell communication and signaling : CCS · 2025Article
- IL-33/NF-κB/ST2L/Rab37 positive-feedback loop promotes M2 macrophage to limit chemotherapeutic efficacy in lung cancer.Cell death & disease · 2024Article
- Macrophages Orchestrate Airway Inflammation, Remodeling, and Resolution in Asthma.International journal of molecular sciences · 2023Review
- Pulmonary Macrophage Cell Death in Lung Health and Disease.American journal of respiratory cell and molecular biology · 2021Review
- IL-33-ST2 axis regulates myeloid cell differentiation and activation enabling effective club cell regeneration.Nature communications · 2020Article
- International expert consensus on the management of allergic rhinitis (AR) aggravated by air pollutants: Impact of air pollution on patients with AR: Current knowledge and future strategies.The World Allergy Organization journal · 2020Article
- Type 2 innate lymphoid cells participate in IL-33-stimulated Th2-associated immune response in chronic obstructive pulmonary disease.Experimental and therapeutic medicine · 2019Article
- Genes and Pathways Regulating Decline in Lung Function and Airway Remodeling in Asthma.Allergy, asthma & immunology research · 2019Review
- IL-4 receptor dependent expansion of lung CD169+ macrophages in microfilaria-driven inflammation.PLoS neglected tropical diseases · 2019Article
- Antigen-specific airway IL-33 production depends on FcγR-mediated incorporation of the antigen by alveolar macrophages in sensitized mice.Immunology · 2018Article
- Potential Role of Interleukin-25/Interleukin-33/Thymic Stromal Lymphopoietin-Fibrocyte Axis in the Pathogenesis of Allergic Airway Diseases.Chinese medical journal · 2018Review
- Tolerogenic Dendritic Cells Reduce Airway Inflammation in a Model of Dust Mite Triggered Allergic Inflammation.Allergy, asthma & immunology research · 2018Article
- Anti-IL-33 Antibody Has a Therapeutic Effect in an Atopic Dermatitis Murine Model Induced by 2, 4-Dinitrochlorobenzene.Inflammation · 2018Article
- Alveolar Macrophages in the Resolution of Inflammation, Tissue Repair, and Tolerance to Infection.Frontiers in immunology · 2018Review
- Potential new targets for drug development in severe asthma.The World Allergy Organization journal · 2018Review
- Research highlights from the 2017 ERS International Congress: airway diseases in focus.ERJ open research · 2018Review
- The Potential for Emerging Microbiome-Mediated Therapeutics in Asthma.Current allergy and asthma reports · 2017Review
- Understanding Interleukin 33 and Its Roles in Eosinophil Development.Frontiers in medicine · 2017Review
- Geometrical Frustration in Interleukin-33 Decouples the Dynamics of the Functional Element from the Folding Transition State Ensemble.PloS one · 2015Article
- Vaccination against IL-33 Inhibits Airway Hyperresponsiveness and Inflammation in a House Dust Mite Model of Asthma.PloS one · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Allergen-specific IgE has long been regarded as a major molecular component of allergic asthma. Additionally, there is increasing evidence of the important roles of interleukin-33 (IL-33) in the disease. Here, we show that IL-33 and alveolar macrophages play essential roles in the exacerbation of IgE-mediated airway inflammation and remodelling. BALB/c mice passively sensitized with ovalbumin (OVA)-specific IgE monoclonal antibody (mAb) were challenged with OVA seven times intratracheally. The seventh challenge exacerbated airway inflammation and remodelling compared with the fourth challenge; furthermore, markedly increased expression of IL-33 in the lungs was observed at the fourth and seventh challenges. When anti-IL-33 or anti-ST2 antibody was administered during the fourth to seventh challenge, airway inflammation and remodelling were significantly inhibited at the seventh challenge. Because increases of IL-33(+) and ST2(+) alveolar macrophages and ST2(+) CD4(+) T cells in the lungs were observed at the fourth challenge, the roles of macrophages and CD4(+) cells were investigated. Depletion of macrophages by 2-chloroadenosine during the fourth to seventh challenge suppressed airway inflammation and remodelling, and IL-33 production in the lung at the seventh challenge; additionally, anti-CD4 mAb inhibited airway inflammation, but not airway remodelling and IL-33 production. Meanwhile, treatment with 2-chloroadenosine or anti-CD4 mAb decreased IL-33-induced airway inflammation in normal mice; airway remodelling was repressed only by 2-chloroadenosine. These results illustrate that macrophage-derived IL-33 contributes to the exacerbation of IgE-mediated airway inflammation by mechanisms associated with macrophages and CD4(+) cells, and airway remodelling through the activation of macrophages.
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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.