{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T23:24:47Z","timestamp":1792106687011,"version":"4.4.0"},"reference-count":45,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2018,2,5]],"date-time":"2018-02-05T00:00:00Z","timestamp":1517788800000},"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":["31570885"],"award-info":[{"award-number":["31570885"]}],"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":["81771679"],"award-info":[{"award-number":["81771679"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Allergy"],"published-print":{"date-parts":[[2018,8]]},"abstract":"Abstract<\/jats:title>Background<\/jats:title>IL<\/jats:styled-content>\u201037 is emerging as an anti\u2010inflammatory cytokine, particularly in innate inflammation. However, the role of IL<\/jats:styled-content>\u201037 in Th2\u2010mediated allergic lung inflammation remains uncertain. We sought to determine the role and the underlying mechanisms of IL<\/jats:styled-content>\u201037 in the development of house dust mites (HDM<\/jats:styled-content>)\u2010induced murine asthma model.<\/jats:p><\/jats:sec>Methods<\/jats:title>We examined the effect of IL<\/jats:styled-content>\u201037 administration during the sensitization or challenge phase on Th2\u2010mediated allergic asthma induced by inhaled HDM<\/jats:styled-content>. Cellular source of CCL<\/jats:styled-content>11 and distribution of IL<\/jats:styled-content>\u201037 receptors, IL<\/jats:styled-content>\u201018R\u03b1 and IL<\/jats:styled-content>\u20101R8, were determined in HDM<\/jats:styled-content>\u2010exposed lungs. Finally, we examined the effect of IL<\/jats:styled-content>\u201037 on CCL<\/jats:styled-content>11 production and STAT<\/jats:styled-content>6 activation in different primary lung structural cell types upon IL<\/jats:styled-content>\u20104\/IL<\/jats:styled-content>\u201013 stimulation.<\/jats:p><\/jats:sec>Results<\/jats:title>IL<\/jats:styled-content>\u201037 had no effect on HDM<\/jats:styled-content> sensitization, but when administrated during the challenge phase, significantly attenuated pulmonary eosinophilia, CCL<\/jats:styled-content>11 production, and airway hyper\u2010reactivity (AHR<\/jats:styled-content>). Interestingly, IL<\/jats:styled-content>\u201037 treatment had no significant effects on lung infiltrating T cells and Th2 cytokine production. Intranasal co\u2010administration of CCL<\/jats:styled-content>11 reversed the inhibiting effect of IL<\/jats:styled-content>\u201037 on HDM<\/jats:styled-content>\u2010induced pulmonary eosinophilia and AHR<\/jats:styled-content>. Furthermore, we demonstrated that CCL<\/jats:styled-content>11 was primarily expressed by fibroblasts and airway smooth muscle cells (AMSC<\/jats:styled-content>), while IL<\/jats:styled-content>\u201037 receptors by tracheobronchial epithelial cells (TEC<\/jats:styled-content>). In vitro study showed that IL<\/jats:styled-content>\u201037 inhibited IL<\/jats:styled-content>\u20104\/IL<\/jats:styled-content>\u201013\u2010induced STAT<\/jats:styled-content>6 activation and CCL<\/jats:styled-content>11 production by fibroblasts and AMSC<\/jats:styled-content>, which was dependent on its direct action on TEC<\/jats:styled-content>. Moreover, cell contact was required for the inhibitory effect of IL<\/jats:styled-content>\u201037\u2010treated TEC<\/jats:styled-content>.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>IL<\/jats:styled-content>\u201037 attenuates HDM<\/jats:styled-content>\u2010induced asthma, possibly by inhibiting IL<\/jats:styled-content>\u20104\/IL<\/jats:styled-content>\u201013\u2010induced CCL<\/jats:styled-content>11 production by fibroblasts and AMSC<\/jats:styled-content> via its direct act on TEC<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/all.13395","type":"journal-article","created":{"date-parts":[[2018,1,10]],"date-time":"2018-01-10T17:23:54Z","timestamp":1515605034000},"page":"1642-1652","source":"Crossref","is-referenced-by-count":52,"title":["IL<\/scp>\u201037 inhibits IL<\/scp>\u20104\/IL<\/scp>\u201013\u2010induced CCL<\/scp>11 production and lung eosinophilia in murine allergic 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Medical Sciences Fudan University Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"X.","family":"Cheng","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology and Parasitology School of Basic Medical Sciences Fudan University Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Q.","family":"Leng","sequence":"additional","affiliation":[{"name":"CAS Key Laboratory of Molecular Virology & Immunology Institute Pasteur of Shanghai Chinese Academy of Sciences Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5288-9786","authenticated-orcid":false,"given":"R.","family":"He","sequence":"additional","affiliation":[{"name":"Department of Immunology School of Basic Medical Sciences Fudan University Shanghai China"},{"name":"Department of Laboratory Animal Science Fudan University Shanghai China"},{"name":"State Key Laboratory of Medical Neurobiology 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