{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T22:32:27Z","timestamp":1791930747189,"version":"4.3.4"},"reference-count":41,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2019,12,18]],"date-time":"2019-12-18T00:00:00Z","timestamp":1576627200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100003130","name":"Fonds Wetenschappelijk Onderzoek","doi-asserted-by":"publisher","award":["1S20418N"],"award-info":[{"award-number":["1S20418N"]}],"id":[{"id":"10.13039\/501100003130","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003132","name":"Agentschap voor Innovatie door Wetenschap en Technologie","doi-asserted-by":"publisher","award":["TBM project 130260"],"award-info":[{"award-number":["TBM project 130260"]}],"id":[{"id":"10.13039\/501100003132","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Allergy"],"published-print":{"date-parts":[[2020,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Increased epithelial permeability has been reported in allergic rhinitis, with histamine and type\u20102 inflammation being responsible for tight junction dysfunction. The impact of an epithelial barrier defect on allergic sensitization and mast cell (MC) degranulation remains speculative.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Transepithelial passage of allergens was evaluated on primary human nasal epithelial cell cultures. Active sensitization was attempted by repeated intranasal ovalbumin (OVA) applications in Na\u00efve mice. In a passive sensitization model, mice were injected with IgE to\n                      <jats:italic>Dermatophagoides pteronyssinus<\/jats:italic>\n                      (r\n                      <jats:italic>Der p<\/jats:italic>\n                      )2 and then exposed intranasally to the allergen. Chitosan was used to disrupt nasal epithelial integrity\n                      <jats:italic>in vitro<\/jats:italic>\n                      and\n                      <jats:italic>in vivo<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Chitosan strongly reduced transepithelial electrical resistance and facilitated transepithelial allergen passage in cultured primary nasal epithelial cells.\n                      <jats:italic>In vivo<\/jats:italic>\n                      , intranasal chitosan affected occludin expression and facilitated allergen passage. After epithelial barrier disruption, intranasal OVA application induced higher OVA\u2010specific IgG1 and total IgE in serum, and increased eosinophilia and interleukin\u20105 in bronchoalveolar lavage (BAL) compared to sham\u2010OVA mice. Chitosan exposure, prior to r\n                      <jats:italic>Der p<\/jats:italic>\n                      2 allergen challenge in passively sensitized mice, resulted in increased \u03b2\u2010hexosaminidase levels in serum and BAL compared to sham\u2010r\n                      <jats:italic>Der p<\/jats:italic>\n                      2 mice. Intranasal treatment with the synthetic glucocorticoid fluticasone propionate prevented chitosan\u2010induced barrier dysfunction, allergic sensitization, and MC degranulation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Epithelial barrier dysfunction facilitates transepithelial allergen passage, allergic sensitization, and allergen\u2010induced MC degranulation even in the absence of inflammatory environment. These results emphasize the crucial role of an intact epithelial barrier in prevention of allergy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/all.14132","type":"journal-article","created":{"date-parts":[[2019,11,26]],"date-time":"2019-11-26T11:50:07Z","timestamp":1574769007000},"page":"1155-1164","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":78,"title":["Nasal epithelial barrier dysfunction increases sensitization and mast cell degranulation in the absence of allergic inflammation"],"prefix":"10.1111","volume":"75","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3649-1131","authenticated-orcid":false,"given":"Inge","family":"Kortekaas Krohn","sequence":"first","affiliation":[{"name":"Department of Microbiology, Immunology and Transplantation Allergy and Clinical Immunology Research group KU Leuven Leuven 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