{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T03:34:30Z","timestamp":1790134470656,"version":"4.0.1"},"reference-count":35,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2017,3,13]],"date-time":"2017-03-13T00:00:00Z","timestamp":1489363200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000272","name":"National Institute for Health Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000272","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2017,6]]},"abstract":"Summary<\/jats:title>Background<\/jats:title>Mild asthmatics who smoke cigarettes may develop unstable disease and neutrophilic infiltration of the airways, features more usually associated with severe asthmatic disease. The mechanisms giving rise to this response remain unclear.<\/jats:p><\/jats:sec>Objective<\/jats:title>To address the hypothesis that smoking increases bronchial mucosal production of IL<\/jats:styled-content>\u201017A which acts on bronchial epithelial cells directly and in concert with other environmental stimuli to induce the production of IL<\/jats:styled-content>\u20106 and neutrophil chemotaxins.<\/jats:p><\/jats:sec>Methods<\/jats:title>IL<\/jats:styled-content>\u201017A, IL<\/jats:styled-content>\u20108, IL<\/jats:styled-content>\u20106, neutrophils and eosinophils were detected and quantified by immunohistochemistry in endobronchial biopsy sections from smoking and non\u2010smoking asthmatics. Human tracheal epithelial cells (HTE<\/jats:styled-content>pC) were cultured with IL<\/jats:styled-content>\u201017A in the presence\/absence of cigarette smoke extract (CSE<\/jats:styled-content>) and aeroallergens lacking intrinsic protease activity, and IL<\/jats:styled-content>\u20106 and IL<\/jats:styled-content>\u20108 production measured in vitro<\/jats:italic>.<\/jats:p><\/jats:sec>Results<\/jats:title>Expression of IL<\/jats:styled-content>\u201017A, IL<\/jats:styled-content>\u20106 and IL<\/jats:styled-content>\u20108 and neutrophil numbers was significantly elevated in the bronchial mucosa of the asthmatic smokers compared to the non\u2010smokers. Expression of IL<\/jats:styled-content>\u201017A correlated with that of IL<\/jats:styled-content>\u20108 and neutrophil numbers. In the smoking asthmatics, eosinophil numbers also correlated with expression of IL<\/jats:styled-content>\u20108 and IL<\/jats:styled-content>\u201017A. Exposure of HTE<\/jats:styled-content>pC cells to both CSE<\/jats:styled-content> and IL<\/jats:styled-content>\u201017A increased expression of IL<\/jats:styled-content>\u20106 and IL<\/jats:styled-content>\u20108 in a concentration\u2010dependent and synergistic manner. Co\u2010stimulation with CSE<\/jats:styled-content>, IL<\/jats:styled-content>\u201017A and aeroallergens further increased IL<\/jats:styled-content>\u20106 and IL<\/jats:styled-content>\u20108 production synergistically.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>The data support the hypothesis that asthmatic smokers develop neutrophilic inflammation of the airways propagated at least partly by smoke\u2010induced production of IL<\/jats:styled-content>\u201017A which together with smoke and other environmental stimuli acts on airways epithelial cells to induce neutrophil chemotaxins.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cea.12907","type":"journal-article","created":{"date-parts":[[2017,2,17]],"date-time":"2017-02-17T06:26:54Z","timestamp":1487312814000},"page":"740-750","source":"Crossref","is-referenced-by-count":54,"title":["Cigarette smoking increases bronchial mucosal IL\u201017A expression in asthmatics, which acts in concert with environmental aeroallergens to engender neutrophilic inflammation"],"prefix":"10.1111","volume":"47","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3656-939X","authenticated-orcid":false,"given":"L. Q. C.","family":"Siew","sequence":"first","affiliation":[{"name":"Division of Asthma, Allergy and Lung Biology MRC\u2010Asthma UK Centre for Allergic Mechanisms of Asthma Guy's Hospital King's College London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.\u2010Y.","family":"Wu","sequence":"additional","affiliation":[{"name":"Division of Asthma, Allergy and Lung Biology MRC\u2010Asthma UK Centre for Allergic Mechanisms of Asthma Guy's Hospital King's College London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Ying","sequence":"additional","affiliation":[{"name":"Division of Asthma, Allergy and Lung Biology MRC\u2010Asthma UK Centre for Allergic Mechanisms of Asthma Guy's Hospital King's College London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. 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