Eosinophil-derived interleukin-24 compromises epithelial integrity and aggravates airway remodeling in mouse models of allergic asthma

Yi-Rou Wu, Chung-Hsi Hsing, Chiao-Juno Chiu, Bor-Luen Chiang and Yu-Hsiang Hsu ()
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Yi-Rou Wu: National Cheng Kung University
Chung-Hsi Hsing: Chi Mei Medical Center
Chiao-Juno Chiu: National Cheng Kung University
Bor-Luen Chiang: National Taiwan University Hospital
Yu-Hsiang Hsu: National Cheng Kung University

Nature Communications, 2025, vol. 16, issue 1, 1-18

Abstract: 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.

Date: 2025
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DOI: 10.1038/s41467-025-64302-4

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