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However, the mechanisms driving tight junctions (TJs) disruption remain unclear. We aimed to elucidate the role of IL\u201013 in TJs breakdown and epithelial remodeling, and to evaluate whether dupilumab can restore epithelial integrity under Type\u20102 inflammatory conditions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Differentially expressed TJs\u2010related genes were identified by integrating the GSE136825 dataset with clinical samples from 23 healthy controls and 73 CRSwNP patients. The effects of IFN\u2010\u03b3, IL\u201013, IL\u201017A, and dupilumab on epithelial barrier function and claudin\u201010 (CLDN10) expression were investigated in seven human nasal epithelial cells using transepithelial electrical resistance (TER), RT\u2010qPCR, WB, and immunofluorescence. Statistical analyses were performed using the chi\u2010square test, one\u2010way ANOVA, Wilcoxon signed\u2010rank test, and Spearman's rank correlation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      CLDN10 was identified as the most significantly downregulated TJs in CRSwNP and negatively correlated with eosinophil infiltration (\n                      <jats:italic>r<\/jats:italic>\n                      = \u22120.4414,\n                      <jats:italic>p<\/jats:italic>\n                      &lt; 0.0001). In vitro, IL\u201013 markedly reduced CLDN10 and TER levels, and induced epithelial remodeling with fewer club cells and ciliated cells and more goblet cells (all\n                      <jats:italic>p<\/jats:italic>\n                      &lt; 0.05). Additionally, dupilumab effectively mitigated IL\u201013\u2010induced CLDN10 loss, restored barrier integrity, and normalized epithelial alarmins, including IL\u201025 and TSLP expression (all\n                      <jats:italic>p<\/jats:italic>\n                      &lt; 0.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>IL\u201013\u2010driven Type\u20102 inflammation disrupts nasal epithelial barrier integrity by downregulating CLDN10 and altering epithelial cell differentiation. Dupilumab counteracts these effects by restoring CLDN10 expression and epithelial barrier function, highlighting CLDN10 as a crucial mediator of barrier dysfunction and a potential therapeutic target in CRSwNP.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/alr.70179","type":"journal-article","created":{"date-parts":[[2026,5,6]],"date-time":"2026-05-06T16:01:46Z","timestamp":1778083306000},"page":"1115-1124","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Dupilumab Alleviates IL\u201013\u2010Induced Nasal Epithelial Barrier Dysfunction by Regulating Claudin\u201010 Expression"],"prefix":"10.1002","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5222-0599","authenticated-orcid":false,"given":"Zhi\u2010Qun","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Allergy, The First Affiliated Hospital, Jiangxi Medical College Nanchang University  Nanchang 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