{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T22:32:25Z","timestamp":1791930745445,"version":"4.3.4"},"reference-count":53,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2019,8,12]],"date-time":"2019-08-12T00:00:00Z","timestamp":1565568000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["31672295"],"award-info":[{"award-number":["31672295"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Int Forum Allergy Rhinol"],"published-print":{"date-parts":[[2019,11]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Interleukin (IL)\u201017A is involved in the pathogenesis of allergic rhinitis (AR). Increased expression of IL\u201017A is correlated with disease severity and nasal eosinophilia. However, the molecular mechanisms by which IL\u201017A contributes to T\u2010helper 2 cytokine IL\u201013\u2012driven pathology in AR remain unclear. We sought to obtain mechanistic insight into how IL\u201017A and IL\u201013 regulate the epithelial production of eotaxin\u20103 representing eosinophilic inflammation in AR.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Human nasal epithelial cells (HNECs) from AR patients were cultured and stimulated with IL\u201017A, IL\u201013, or IL\u201017A and IL\u201013. Phosphorylated signal transducer activator of transcription 6 (p\u2010STAT6) and suppressor of cytokine signaling 1 (SOCS1) in HNECs were assayed using Western blotting. Immunocytochemistry was used to determine p\u2010STAT6\u2012positive expression in the cells. Eotaxin\u20103 expression in the cells and culture supernatants was evaluated using real\u2010time polymerase chain reaction and enzyme\u2010linked immunosorbent assays.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Stimulation with IL\u201013 alone induced STAT6 phosphorylation and promoted p\u2010STAT6 nuclear translocation, leading to eotaxin\u20103 production by HNECs. These effects were further enhanced by cotreatment with IL\u201013 and IL\u201017A, whereas IL\u201017A alone had no impact on STAT6 or eotaxin\u20103 expression. Incubation with IL\u201017A or IL\u201013 increased the level of SOCS1 protein in the cells, whereas the addition of IL\u201017A attenuated IL\u201013\u2012induced SOCS1 expression.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>IL\u201017A potentiated IL\u201013\u2012driven STAT6 activation through the downregulation of SOCS1 expression, leading to enhancement of eotaxin\u20103 production by HNECs. These factors contributed to eosinophilic inflammation in AR.<\/jats:p><\/jats:sec>","DOI":"10.1002\/alr.22382","type":"journal-article","created":{"date-parts":[[2019,8,12]],"date-time":"2019-08-12T14:58:38Z","timestamp":1565621918000},"page":"1327-1333","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Interleukin\u201017A potentiates interleukin\u201013\u2012induced eotaxin\u20103 production by human nasal epithelial cells from patients with allergic rhinitis"],"prefix":"10.1002","volume":"9","author":[{"given":"Wei Wei","family":"Wang","sequence":"first","affiliation":[{"name":"Schools of Medicine and Nursing Sciences Huzhou University  Zhejiang PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kai","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Pathology Huzhou Maternity and Child Health Care Hospital  Zhejiang PR 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