{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T07:54:42Z","timestamp":1791446082520,"version":"4.3.3"},"reference-count":39,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T00:00:00Z","timestamp":1787788800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T00:00:00Z","timestamp":1787788800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100008307","name":"Promedica Stiftung","doi-asserted-by":"publisher","award":["1515\/M"],"award-info":[{"award-number":["1515\/M"]}],"id":[{"id":"10.13039\/501100008307","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001711","name":"Schweizerischer Nationalfonds zur F\u00f6rderung der Wissenschaftlichen Forschung","doi-asserted-by":"publisher","award":["310030_219210"],"award-info":[{"award-number":["310030_219210"]}],"id":[{"id":"10.13039\/501100001711","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001711","name":"Schweizerischer Nationalfonds zur F\u00f6rderung der Wissenschaftlichen Forschung","doi-asserted-by":"publisher","award":["32003B_204751\/1"],"award-info":[{"award-number":["32003B_204751\/1"]}],"id":[{"id":"10.13039\/501100001711","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Allergy"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Eosinophilic esophagitis (EoE) is a chronic immune\u2010mediated disease characterized by symptoms of esophageal dysfunction, such as dysphagia and food impaction, as well as eosinophilic inflammation and impaired epithelial barrier integrity, which promotes allergen influx. Environmental exposures that weaken the esophageal barrier, including surfactants found in personal care products such as sodium dodecyl sulfate (SDS) and cocamidopropyl betaine (CAPB), have been proposed as contributors to disease susceptibility. However, their direct effects on esophageal epithelial barrier function and associated molecular responses remain insufficiently characterized.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We investigated the molecular and functional consequences of SDS and CAPB exposure in primary EoE\u2010derived esophageal organoids and air\u2010liquid interface cultures derived from biopsy tissue samples. We conducted transepithelial electrical resistance (TEER) measurements, paracellular flux assays, RNA sequencing, targeted and untargeted proteomics, and immunofluorescence imaging.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Treatment of esophageal organoids with SDS or CAPB (0\u2013100\u2009\u03bcg\/mL) caused dose\u2010dependent cytotoxicity and barrier disruption, with SDS producing stronger effects. At 12.5\u2009\u03bcg\/mL, viability declined to ~30% with SDS versus ~60% with CAPB, accompanied by greater TEER reduction and ~2\u2010fold higher permeability. RNA\u2010seq of organoids exposed to 12.5\u2009\u03bcg\/mL for 24\u2009h showed distinct transcriptomic clustering, with 2749 shared and &gt;\u20091500 surfactant\u2010specific differentially expressed genes, indicating broad epithelial remodeling, cell\u2010cycle suppression, and stress responses, more pronounced under SDS. SDS preferentially activated inflammatory and innate immune pathways, which was supported by proteomic detection of elevated cytokines (TNF, IL\u20108, IL\u201018, etc.). Both surfactants induced keratinization, epidermal cell differentiation, and partial epithelial\u2010mesenchymal transition signatures, including increased vimentin without E\u2010cadherin loss.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These findings demonstrate that common surfactants can induce coordinated epithelial stress responses in esophageal tissue models and may act as environmental aggravating factors in EoE at relatively low doses. This work underscores the need to consider mucosal exposure to consumer product ingredients in the context of epithelial barrier disorders, particularly surfactants such as SDS and CAPB, and supports efforts to refine formulations to minimize epithelial damage.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/all.70490","type":"journal-article","created":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T09:13:38Z","timestamp":1787822018000},"page":"3659-3672","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Pathways of Epithelial Barrier Breakdown and Remodeling in Esophageal Organoids by Commonly Used Surfactants"],"prefix":"10.1111","volume":"81","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6077-0478","authenticated-orcid":false,"given":"Ozge","family":"Ardicli","sequence":"first","affiliation":[{"name":"Swiss Institute of Allergy and Asthma Research (SIAF) University of Zurich  Davos 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