{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T02:40:53Z","timestamp":1772160053967,"version":"3.50.1"},"reference-count":42,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2016,3,29]],"date-time":"2016-03-29T00:00:00Z","timestamp":1459209600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001734","name":"K\u00f8benhavns Universitet","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001734","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2016,4]]},"abstract":"Summary<\/jats:title>\n \n Background<\/jats:title>\n \n IL<\/jats:styled-content>\n \u201033 represents a potential link between the airway epithelium and induction of a Th2\u2010type inflammatory response in asthma. However, the association with markers of eosinophilic airway inflammation has not previously been reported in patients with steroid\u2010free asthma.\n <\/jats:p>\n <\/jats:sec>\n \n Aim<\/jats:title>\n \n To describe the relationship between airway\n IL<\/jats:styled-content>\n \u201033 and markers of eosinophilic airway inflammation, as well potential triggers of\n IL<\/jats:styled-content>\n \u201033, in mild, steroid\u2010free asthma.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n IL<\/jats:styled-content>\n \u201033\n mRNA<\/jats:styled-content>\n expression and\n IL<\/jats:styled-content>\n \u201033 immunoreactivity were measured in bronchial biopsies from patients with asthma untreated with inhaled steroids and healthy individuals. Furthermore, fractional exhaled nitric oxide (Fe\n NO<\/jats:styled-content>\n ) and eosinophils in sputum and\n BAL<\/jats:styled-content>\n were measured, as well as airway hyperresponsiveness to mannitol and methacholine. Epithelial integrity was assessed by computerized image analysis on haematoxylin\u2010stained sections, and\n TLR mRNA<\/jats:styled-content>\n expression by\n PCR<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n A total of 23 patients with asthma and 10 healthy individuals were examined (age: 24\u00a0years (20\u201340); females: 53%). The level of\n IL<\/jats:styled-content>\n \u201033\n mRNA<\/jats:styled-content>\n expression was significantly higher in patients with asthma compared to healthy individuals (Median (\n IQR<\/jats:styled-content>\n ) 1.12 (0.78) vs. 0.86,\n P\u00a0<\/jats:italic>\n =\n \u00a0<\/jats:italic>\n 0.04). There was a positive correlation between\n IL<\/jats:styled-content>\n \u201033\n mRNA<\/jats:styled-content>\n expression and the level of Fe\n NO<\/jats:styled-content>\n (\n r<\/jats:italic>\n \u00a0=\u00a00.56,\n P\u00a0<\/jats:italic>\n =\n \u00a0<\/jats:italic>\n 0.01), whereas there was no association with airway or blood eosinophils.\n IL<\/jats:styled-content>\n \u201033 expression was unrelated to loss of epithelial integrity, but correlated with an increased expression of\n TLR<\/jats:styled-content>\n 2 and\n TLR<\/jats:styled-content>\n 4 (\n TLR<\/jats:styled-content>\n 2:\n r<\/jats:italic>\n \u00a0=\u00a00.47,\n P\u00a0<\/jats:italic>\n =\n \u00a0<\/jats:italic>\n 0.04;\n TLR<\/jats:styled-content>\n 4: 0.68,\n P\u00a0<\/jats:italic>\n <\n \u00a0<\/jats:italic>\n 0.001), as well allergy to house dust mites (\n HDM<\/jats:styled-content>\n s).\n <\/jats:p>\n <\/jats:sec>\n \n Conclusion<\/jats:title>\n \n In mild untreated asthma, the expression of\n IL<\/jats:styled-content>\n \u201033\n mRNA<\/jats:styled-content>\n in bronchial mucosa is related to innate immune activation and allergic sensitization to\n HDM<\/jats:styled-content>\n , rather than epithelial damage, and correlates with Fe\n NO<\/jats:styled-content>\n . These findings suggest that in mild allergic asthma,\n IL<\/jats:styled-content>\n \u201033 may represent a link between innate immune activation and Fe\n NO<\/jats:styled-content>\n production.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/cea.12702","type":"journal-article","created":{"date-parts":[[2016,1,10]],"date-time":"2016-01-10T11:13:06Z","timestamp":1452424386000},"page":"564-574","source":"Crossref","is-referenced-by-count":16,"title":["IL<\/scp>\n \u201033 is related to innate immune activation and sensitization to\n HDM<\/scp>\n in mild steroid\u2010free asthma"],"prefix":"10.1111","volume":"46","author":[{"given":"C.","family":"Porsbjerg","sequence":"first","affiliation":[{"name":"Respiratory Research Unit Bispebjerg Hospital Copenhagen Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Baines","sequence":"additional","affiliation":[{"name":"Centre for Asthma and Respiratory Disease The University of Newcastle Newcastle NSW Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P.","family":"Gibson","sequence":"additional","affiliation":[{"name":"Centre for Asthma and Respiratory Disease The University of Newcastle Newcastle NSW Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"Bergqvist","sequence":"additional","affiliation":[{"name":"Respiratory Medicine and Allergology and Experimental Medical Science Lund University Lund Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. 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