{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,3]],"date-time":"2026-07-03T21:26:11Z","timestamp":1783113971659,"version":"3.54.6"},"reference-count":39,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T00:00:00Z","timestamp":1772150400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T00:00:00Z","timestamp":1772150400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100019212","name":"American Academy of Allergy, Asthma and Immunology Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100019212","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Pediatric Allergy Immunology"],"published-print":{"date-parts":[[2026,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Eosinophilic esophagitis (EoE) is a chronic allergic disorder driven by type 2 inflammation, characterized by eosinophilic infiltration and esophageal epithelial abnormalities, including barrier dysfunction, basal cell hyperplasia, epithelial thickening, and loss of differentiation. Although proton pump inhibitor (PPI) therapy is frequently employed in the management of EoE and is known to reduce esophageal eosinophilia, improve barrier function, and exert anti\u2010inflammatory effects, the precise mechanism by which PPIs modulate type 2 inflammation and epithelial integrity remains incompletely understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Air\u2010liquid interface culture of esophageal epithelial cells was used to investigate the impact of the PPI omeprazole on barrier integrity in IL\u201013\u2010treated cultures. Epithelial chemokine secretion was assessed following stimulation with IL\u201013 and omeprazole, and eosinophil migration from healthy human donors was evaluated using 3\u2009\u03bcm pore\u2010sized transwells. A co\u2010culture system of epithelial cells and eosinophils was used to examine chemokine secretion, eosinophil adhesion, and activation marker expression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Omeprazole treatment of IL\u201013\u2010treated air\u2010liquid interface (ALI) cultures restored barrier integrity compared with IL\u201013\u2010treated ALI cultures and resulted in 186 differentially expressed genes. Omeprazole treatment reduced STAT6 phosphorylation, downregulated calpain 14 expression, and upregulated desmoglein\u20101 in IL\u201013\u2010treated ALI samples. IL\u201013 treatment induced upregulation of Eotaxin\u20103, CXCL10, and periostin, which were downregulated by omeprazole. Eosinophils co\u2010cultured with human esophageal epithelial cells in the presence of omeprazole had diminished CD11b, CD18, and CD69 expression compared to those cultured with IL\u201013 alone, and less eotaxin\u20103, CXCL10, CCL2, and CCL4 were recovered from the co\u2010culture media.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Omeprazole diminished the effects of IL\u201013 in both the epithelial air\u2010liquid interface model and eosinophil\u2010epithelial co\u2010cultures, alleviating barrier dysfunction, chemokine expression, and the upregulation of eosinophil adhesion markers.<\/jats:p>\n                  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