{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T19:04:08Z","timestamp":1789758248829,"version":"4.0.1"},"reference-count":35,"publisher":"European Respiratory Society (ERS)","issue":"2","license":[{"start":{"date-parts":[[2020,9,9]],"date-time":"2020-09-09T00:00:00Z","timestamp":1599609600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.ersjournals.com\/user-licence"}],"funder":[{"DOI":"10.13039\/100007013","name":"F. Hoffmann-La Roche","doi-asserted-by":"publisher","award":["HLR-14"],"award-info":[{"award-number":["HLR-14"]}],"id":[{"id":"10.13039\/100007013","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Netherlands Lung Foundation","award":["LF4.1.18.226"],"award-info":[{"award-number":["LF4.1.18.226"]}]},{"name":"Netherlands Lung Foundation","award":["LF5.1.14.020"],"award-info":[{"award-number":["LF5.1.14.020"]}]}],"content-domain":{"domain":["publications.ersnet.org"],"crossmark-restriction":true},"short-container-title":["Eur Respir J"],"accepted":{"date-parts":[[2020,8,17]]},"published-print":{"date-parts":[[2021,2]]},"abstract":"<jats:p>\n                    Periostin (POSTN) may serve as a biomarker for Type-2 mediated eosinophilic airway inflammation in asthma. We hypothesised that a Type-2 cytokine, interleukin (IL)-13, induces airway epithelial expression of\n                    <jats:italic>POSTN<\/jats:italic>\n                    , which in turn contributes to epithelial changes observed in asthma.\n                  <\/jats:p>\n                  <jats:p>\n                    We studied the effect of IL-13 on\n                    <jats:italic>POSTN<\/jats:italic>\n                    expression in BEAS-2B and air\u2013liquid interface differentiated primary bronchial epithelial cells (PBECs). Additionally, the effects of recombinant human POSTN on epithelial-to-mesenchymal transition (EMT) markers and mucin genes were assessed.\n                    <jats:italic>POSTN<\/jats:italic>\n                    single cell gene expression and protein levels were analysed in bronchial biopsies and induced sputum from asthma patients and healthy controls.\n                  <\/jats:p>\n                  <jats:p>\n                    IL-13 increased\n                    <jats:italic>POSTN<\/jats:italic>\n                    expression in both cell types and this was accompanied by EMT-related features in BEAS-2B. In air\u2013liquid interface differentiated PBECs, IL-13 increased POSTN basolateral and apical release. Apical administration of POSTN increased the expression of\n                    <jats:italic>MMP-9<\/jats:italic>\n                    ,\n                    <jats:italic>MUC5B<\/jats:italic>\n                    and\n                    <jats:italic>MUC5AC<\/jats:italic>\n                    . In bronchial biopsies,\n                    <jats:italic>POSTN<\/jats:italic>\n                    expression was mainly confined to basal epithelial cells, ionocytes, endothelial cells and fibroblasts, showing higher expression in basal epithelial cells from asthma patients\n                    <jats:italic>versus<\/jats:italic>\n                    those from controls. A higher level of POSTN protein expression in epithelial and subepithelial layers was confirmed in bronchial biopsies from asthma patients when compared to healthy controls. Although sputum POSTN levels were not higher in asthma, levels correlated with eosinophil numbers and with the coughing-up of mucus.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>POSTN<\/jats:italic>\n                    expression is increased by IL-13 in bronchial epithelial cells and is higher in bronchial biopsies from asthma patients. This may have important consequences, as administration of POSTN increases epithelial expression of mucin genes, supporting the relationship of POSTN with Type-2 mediated asthma and mucus secretion.\n                  <\/jats:p>","DOI":"10.1183\/13993003.01286-2020","type":"journal-article","created":{"date-parts":[[2020,9,10]],"date-time":"2020-09-10T00:25:29Z","timestamp":1599697529000},"page":"2001286","update-policy":"https:\/\/doi.org\/10.1183\/ers-crossmark-policy","source":"Crossref","is-referenced-by-count":52,"title":["Periostin: contributor to abnormal airway epithelial function in asthma?"],"prefix":"10.1183","volume":"57","author":[{"given":"Janette K.","family":"Burgess","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marnix 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