ArticleJournal of rhinology : official journal of the Korean Rhinologic Society2026
IL-5Rα-Mediated Signaling in Eosinophils May Contribute to the Epithelial-Mesenchymal Transition in Eosinophilic Chronic Rhinosinusitis With Nasal Polyps.
Article in Journal of rhinology : official journal of the Korean Rhinologic Society, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BACKGROUND AND
objectivesEosinophilic chronic rhinosinusitis with nasal polyps (ECRSwNP) is characterized by type 2 inflammation, prominent eosinophil accumulation, and enhanced epithelial-mesenchymal transition (EMT). Although interleukin (IL)-5 plays a central role in eosinophil differentiation and activation, its involvement in driving EMT in human nasal epithelial cells (HNECs) remains unclear. This study investigated IL-5 receptor α (IL-5Rα)-mediated signaling and EMT profiles in ECRSwNP, aiming to determine whether IL-5-activated eosinophil-like cells promote EMT in HNECs.
methodsNasal tissues from healthy controls, non-ECRSwNP patients, and ECRSwNP patients (n=12 per group) were analyzed using hematoxylin and eosin staining, quantitative real-time polymerase chain reaction, immunohistochemistry, and Western blotting. HL-60 promyelocytic leukemia cells were differentiated into eosinophil-like cells and subsequently stimulated with IL-5. HNECs were cocultured with undifferentiated HL-60 cells, differentiated HL-60 cells, or IL-5-stimulated differentiated HL-60 cells using a Transwell system. Expression of EMT-related markers was assessed by Western blotting and immunofluorescence.
resultsECRSwNP tissues demonstrated markedly increased eosinophil infiltration, elevated IL-4 and IL-5 transcript levels, and significantly higher expression of IL-5Rα, phosphorylated Janus kinase 2 (JAK2), and phosphorylated signal transducer and activator of transcription 5 (STAT5) compared with controls and non-ECRSwNP tissues. EMT-associated changes, characterized by reduced E-cadherin and increased vimentin expression, were most pronounced in ECRSwNP. In vitro, IL-5 stimulation enhanced IL-5Rα expression, activated JAK2/STAT5 signaling, and increased secretion of eosinophil-associated mediators in differentiated HL-60 cells. Co-culture with IL-5-stimulated eosinophil-like cells induced EMT in HNECs, whereas unstimulated HL-60 cells exerted minimal effects.
conclusionIL-5Rα-mediated signaling is upregulated in ECRSwNP and may contribute to EMT through eosinophil-dependent mechanisms. IL-5-activated eosinophils promote EMT-related changes in HNECs, providing a mechanistic link between type 2 inflammation and epithelial remodeling. These findings suggest that IL-5Rα signaling may represent a potential therapeutic target for modulating tissue remodeling in ECRSwNP.
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