{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,5]],"date-time":"2026-06-05T23:11:51Z","timestamp":1780701111781,"version":"3.54.1"},"reference-count":51,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2024,4,19]],"date-time":"2024-04-19T00:00:00Z","timestamp":1713484800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2024,4,19]],"date-time":"2024-04-19T00:00:00Z","timestamp":1713484800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100017950","name":"Shanghai Municipal Health Commission","doi-asserted-by":"publisher","award":["SHWSRS(2023)62"],"award-info":[{"award-number":["SHWSRS(2023)62"]}],"id":[{"id":"10.13039\/100017950","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82071014"],"award-info":[{"award-number":["82071014"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82271137"],"award-info":[{"award-number":["82271137"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82000951"],"award-info":[{"award-number":["82000951"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2024,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>SERPINB2, a biomarker of Type\u20102 (T2) inflammatory processes, has been described in the context of asthma. Chronic rhinosinusitis with nasal polyps (CRSwNP) is also correlated with T2 inflammation and elevated 15LO1 induced by IL\u20104\/13 in nasal epithelial cells. The aim of this study was to evaluate the expression and location of SERPINB2 in nasal epithelial cells (NECs) and determine whether SERPINB2 regulates 15LO1 and downstream T2 markers in NECs via STAT6 signalling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      <jats:italic>SERPINB2<\/jats:italic>\n                      gene expression in bulk and single\u2010cell RNAseq database was analysed by bioinformatics analysis. SERPINB2, 15LO1 and other T2 markers were evaluated from CRSwNP and HCs NECs. The colocalization of SERPINB2 and 15LO1 was evaluated by immunofluorescence. Fresh NECs were cultured at an air\u2010liquid interface with or without IL\u201013, SERPINB2 Dicer\u2010substrate short interfering RNAs (DsiRNAs) transfection, exogenous SERPINB2, 15\u2010HETE recombinant protein and pSTAT6 inhibitors. 15LO1, 15\u2010HETE and downstream T2 markers were analysed by qRT\u2010PCR, western blot and ELISA.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      SERPINB2 expression was increased in eosinophilic nasal polyps compared with that in noneosinophilic nasal polyps and control tissues and positively correlated with 15LO1 and other downstream T2 markers. SERPINB2 was predominantly expressed by epithelial cells in NP tissue and was colocalized with 15LO1. In primary NECs in\u00a0vitro, SERPINB2 expression was induced by IL\u201013. Knockdown or overexpression SERPINB2 decreased or enhanced expression of 15LO1 and 15\u2010HETE in NECs, respectively, in a STAT6\u2010dependent manner.\n                      <jats:italic>SERPINB2<\/jats:italic>\n                      siRNA also inhibited the expression of the 15LO1 downstream genes, such as\n                      <jats:italic>CCL26, POSTN<\/jats:italic>\n                      and\n                      <jats:italic>NOS2<\/jats:italic>\n                      . STAT6 inhibition similarly decreased SERPINB2\u2010induced 15LO1.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>SERPINB2 is increased in NP epithelial cells of eosinophilic CRSwNP (eCRSwNP) and contributes to T2 inflammation via STAT6 signalling. SERPINB2 could be considered a novel therapeutic target for eCRSwNP.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/cea.14484","type":"journal-article","created":{"date-parts":[[2024,4,19]],"date-time":"2024-04-19T06:39:33Z","timestamp":1713508773000},"page":"412-424","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Increased SERPINB2 potentiates 15LO1 expression via STAT6 signalling in epithelial cells in eosinophilic chronic rhinosinusitis with nasal polyps"],"prefix":"10.1111","volume":"54","author":[{"given":"Chunyu","family":"Luo","sequence":"first","affiliation":[{"name":"Department of Otolaryngology\u2010Head and Neck Surgery Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine  Shanghai China"},{"name":"Otolaryngological Institute Shanghai Jiao Tong University  Shanghai China"},{"name":"Shanghai Key Laboratory of Sleep Disordered Breathing  Shanghai 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