{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T13:52:41Z","timestamp":1778680361467,"version":"3.51.4"},"reference-count":40,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2016,5,15]],"date-time":"2016-05-15T00:00:00Z","timestamp":1463270400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100008582","name":"McGill University","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008582","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000024","name":"Canadian Institutes of Health Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000156","name":"Fonds de Recherche du Qu\u00e9bec - Sant\u00e9","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000156","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2016,7]]},"abstract":"Summary<\/jats:title>Background<\/jats:title>Chronic inflammation, typified by increased expression of IL<\/jats:styled-content>\u201017A, together with airway and parenchymal remodelling are features of chronic lung diseases. Emerging evidence suggests that phenotypic heterogeneity of repair and inflammatory capacities of fibroblasts may contribute to the differential structural changes observed in different regions of the lung.<\/jats:p><\/jats:sec>Objective<\/jats:title>To investigate phenotypic differences in parenchymal and bronchial fibroblasts, either in terms of inflammation and remodelling or the ability of these fibroblasts to respond to IL<\/jats:styled-content>\u201017A.<\/jats:p><\/jats:sec>Methods<\/jats:title>Four groups of primary fibroblasts were used: normal human bronchial fibroblast (NHBF<\/jats:styled-content>), normal human parenchymal fibroblast (NHPF<\/jats:styled-content>), COPD<\/jats:styled-content> human bronchial fibroblast (CHBF<\/jats:styled-content>) and COPD<\/jats:styled-content> human parenchymal fibroblast (CHPF<\/jats:styled-content>). Cytokine and extracellular matrix (ECM<\/jats:styled-content>) expression were measured at baseline and after stimulation with IL<\/jats:styled-content>\u201017A. Actinomycin D was used to measure cytokine mRNA<\/jats:styled-content> stability.<\/jats:p><\/jats:sec>Results<\/jats:title>At baseline, we observed higher protein production of IL<\/jats:styled-content>\u20106 in NHPF<\/jats:styled-content> than NHBF<\/jats:styled-content>, but higher levels of IL<\/jats:styled-content>\u20108 and GRO<\/jats:styled-content>\u2010\u03b1 in NHBF<\/jats:styled-content>. IL<\/jats:styled-content>\u201017A induced a higher expression of GRO<\/jats:styled-content>\u2010\u03b1 (CXCL<\/jats:styled-content>1) and IL<\/jats:styled-content>\u20106 in NHPF<\/jats:styled-content> than in NHBF<\/jats:styled-content>, and a higher level of IL<\/jats:styled-content>\u20108 expression in NHBF<\/jats:styled-content>. IL<\/jats:styled-content>\u201017A treatment decreased the mRNA<\/jats:styled-content> stability of IL<\/jats:styled-content>\u20106 in NHBF<\/jats:styled-content> when compared with NHPF<\/jats:styled-content>. CHPF<\/jats:styled-content> expressed higher protein levels of fibronectin, collagen\u2010I and collagen\u2010III<\/jats:styled-content> than CHBF<\/jats:styled-content>, NHBF<\/jats:styled-content> and NHPF<\/jats:styled-content>. IL<\/jats:styled-content>\u201017A increased fibronectin and collagen\u2010III<\/jats:styled-content> protein only in NHPF<\/jats:styled-content> and collagen\u2010III<\/jats:styled-content> protein production in CHBF<\/jats:styled-content> and CHPF<\/jats:styled-content>.<\/jats:p><\/jats:sec>Conclusions and Clinical Relevance<\/jats:title>These findings provide insight into the inflammatory and remodelling processes that may be related to the phenotypic heterogeneity of fibroblasts from airway and parenchymal regions and in their response to IL<\/jats:styled-content>\u201017A.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cea.12744","type":"journal-article","created":{"date-parts":[[2016,4,15]],"date-time":"2016-04-15T10:57:20Z","timestamp":1460717840000},"page":"945-956","source":"Crossref","is-referenced-by-count":18,"title":["Human bronchial and parenchymal fibroblasts display differences in basal inflammatory phenotype and response to IL\u201017A"],"prefix":"10.1111","volume":"46","author":[{"given":"K.","family":"Dessalle","sequence":"first","affiliation":[{"name":"Meakins\u2010Christie Laboratories McGill University Montreal QC Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"V.","family":"Narayanan","sequence":"additional","affiliation":[{"name":"Meakins\u2010Christie Laboratories McGill University Montreal QC Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Kyoh","sequence":"additional","affiliation":[{"name":"Meakins\u2010Christie Laboratories McGill University Montreal QC Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"Mogas","sequence":"additional","affiliation":[{"name":"Meakins\u2010Christie Laboratories McGill University Montreal QC Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A. 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