ArticleEuropean journal of medical research2026
IL-36 participated in airway remodeling in chronic asthma model by inducing epithelial-mesenchymal transition process.
Article in European journal of medical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Anti-Inflammatory Cytokine Signatures in Primary Glaucoma Subtypes: Diagnostic and Pathophysiological Insights From IL-36Ra, IL-37, and IL-38.Journal of ophthalmology · 2026Article
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8 authors.
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Abstract
purposeEpithelial-mesenchymal transition (EMT) is a major pathological characteristic of airway remodelling in severe asthma. Interleukin (IL)-36 belongs to the IL-1 family and is associated with allergic disease, but the role of IL-36 in airway remodelling in asthma remains unclear. We aimed to explore the effect of IL-36 on EMT and to verify whether blocking IL-36-induced EMT can alleviate the airway remodeling in severe asthma.
methodsIn this study, BEAS-2B cells were stimulated with IL-36 receptor (IL-36R) agonist. The expression of epithelial‒mesenchymal transition (EMT) markers and the migration capacity of cells were determined. A chronic asthma mouse model was established to evaluate the effects of IL-36 signalling on airway inflammation and remodelling.
resultsIn vitro, EMT and cell migration in BEAS-2B cells were induced by IL-36. In addition, IL-36 facilitated the phosphorylation of NF-κB and STAT3. In vivo, blocking IL-36R via treatment with an IL-36 receptor antagonist (IL-36Ra) inhibited the infiltration of inflammatory cells, decreased airway hyper-responsiveness (AHR) and alleviated airway remodelling (by inhibiting processes, such as EMT) in asthmatic mice. Compared with the administration of IL-36Ra alone, the coadministration of IL-36R agonist with IL-36Ra restored pathological changes related to airway remodelling.
conclusionsThese data indicated that IL-36 signalling may participate in airway remodelling by inducing EMT. IL-36 may be a new therapeutic target for airway remodelling in severe asthma.
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