{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T15:13:42Z","timestamp":1787238822642,"version":"build-2736575974"},"reference-count":37,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2021,6,19]],"date-time":"2021-06-19T00:00:00Z","timestamp":1624060800000},"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":["81800026"],"award-info":[{"award-number":["81800026"]}],"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":["81670019"],"award-info":[{"award-number":["81670019"]}],"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":["91742108"],"award-info":[{"award-number":["91742108"]}],"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":[[2021,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Airway eosinophilic inflammation is a central feature in asthma which is mainly driven by type 2 response. The expression of galectin\u201013 was up\u2010regulated in a parasitic infection model which is also characterized by type 2 immune response. We hypothesized that galectin\u201013 may be involved in airway eosinophilic inflammation in asthma.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To unveil the role of galectin\u201013 in asthma airway inflammation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We measured galectin\u201013 expressions in bronchial brushings, sputum, and plasma of asthma patients (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a054) and healthy controls (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a015), and analysed the correlations between galectin\u201013 expression and airway eosinophilia. We used human bronchial epithelial cell line 16HBE to investigate the possible mechanism by which galectin\u201013 participates in eosinophilic inflammation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The expression of galectin\u201013 was markedly increased in subjects with asthma compared to controls. Epithelial galectin\u201013 mRNA levels in asthmatic subjects were strongly correlated with eosinophilic airway inflammation (the percentage of sputum eosinophils, the number of eosinophils in bronchial submucosa and FeNO) and the expression of Th2\u00a0signature genes (\n                      <jats:italic>CLCA1<\/jats:italic>\n                      ,\n                      <jats:italic>POSTN<\/jats:italic>\n                      and\n                      <jats:italic>SERPINB2<\/jats:italic>\n                      ). Inhaled corticosteroid (ICS) treatment reduced plasma galectin\u201013 levels, and baseline plasma galectin\u201013\u00a0levels reflect the response to ICS treatment. In cultured 16HBE cells, knockdown of galectin\u201013\u00a0suppressed IL\u201013\u2010stimulated MCP\u20101 and eotaxin\u20101 expression by inhibiting the activation of EGFR and ERK.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions &amp; Clinical Relevance<\/jats:title>\n                    <jats:p>Galectin\u201013 is a novel marker for airway eosinophilia in asthma, and may contribute to allergic airway eosinophilic inflammation by up\u2010regulating the expression of MCP\u20101 and eotaxin\u20101. Plasma galectin\u201013\u00a0levels may be useful for predicting responses to ICS treatment.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/cea.13961","type":"journal-article","created":{"date-parts":[[2021,6,2]],"date-time":"2021-06-02T03:53:39Z","timestamp":1622606019000},"page":"1566-1576","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Increased epithelial galectin\u201013 expression associates with eosinophilic airway inflammation in asthma"],"prefix":"10.1111","volume":"51","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6839-3328","authenticated-orcid":false,"given":"Lingling","family":"Yi","sequence":"first","affiliation":[{"name":"Division of Respiratory and Critical Care Medicine Department of Internal Medicine Tongji Hospital Tongji Medical College Huazhong University of Science and Technology  Wuhan China"},{"name":"Key Laboratory of Respiratory Diseases National Health Commission of 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