ArticleNature communications2025
Eosinophil-derived interleukin-24 compromises epithelial integrity and aggravates airway remodeling in mouse models of allergic asthma.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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
11 citing papers in PubMed.
- The dual pathogenic role of IL-24 in sepsis: Coupling bacterial dissemination with inflammatory amplification as a therapeutic target.Virulence · 2026Article
- Spatially resolved single cell atlas deciphers SAA1 inflammatory epithelial cells.International journal of oral science · 2026Article
- Restoring the Airway Barrier: How Targeting Eosinophilic Inflammation Shapes Epithelial Health and Clinical Remission in Asthma.Diagnostics (Basel, Switzerland) · 2026Review
- Article
- Article
- Reprogramming Inflammatory Macrophages with Specialized Pro-Resolving Lipid Mediators: A Novel Immunotherapeutic Strategy for Asthma.Biomedicines · 2026Review
- The Emerging Role of Ly6G⁺Nur77⁺ Lung Macrophages in Type-2 Allergic Inflammation: A Comprehensive Review on Asthma Pathogenesis.Current allergy and asthma reports · 2026Review
- Review
- Neutrophil extracellular traps induce airway epithelial-mesenchymal transition in a neutrophil-dominant asthmatic murine model through Hedgehog/Gli1 pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Modulation of the NF-κB signaling pathway by the combined strategy of tocilizumab and dexamethasone for asthma therapy.Respiratory research · 2026Article
- Molecular Mechanisms Linking Eosinophils to Lung Function Impairment in Respiratory Diseases.Journal of asthma and allergy · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Asthma is a heterogeneous disease characterized by infiltration of immune cells that interact with epithelial cells and release various factors driving chronic inflammation and airway remodeling. Although monoclonal antibody-based biologics alleviate inflammation, their efficacy in suppressing airway remodeling is limited. Interleukin-24 (IL-24) has been implicated in neutrophilic asthma, but its role in eosinophilic asthma remains unclear. Here, we show that IL-24 is mainly secreted by infiltrating eosinophils in mice with OVA- and HDM-induced asthma-like lung disease models. IL-24 knockout mice exhibit reduced inflammatory responses, alleviated pulmonary fibrosis, improved epithelial integrity, and decreased mucus hypersecretion. Mechanistically, IL-24 activates the CXCL5/CXCR1/CXCR2 axis, enhancing eosinophil recruitment to the lungs. IL-24 disrupts epithelial tight junction integrity, contributing to increased permeability. Furthermore, IL-24 targets airway epithelial cells, promoting EMT-like changes and the secretion of profibrotic mediators, which leads to bronchial wall thickening and pulmonary fibrosis. Therefore, targeting IL-24 holds promise for anti-asthmatic interventions by suppressing inflammation and pathological remodeling.
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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 Socratic graph.