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Sensitization to airborne allergens was examined with skin prick tests (\u22653\u00a0mm wheal) and sensitization to food allergens with measurement of specific IgE (\u22650.35\u00a0kU\/L).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Asthmatics sensitized to food allergens had higher Fe<jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content>, 22.3\u00a0ppb (18.6, 26.7) vs 16.1\u00a0ppb (14.2, 18.2) (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.005), S\u2010<jats:styled-content style=\"fixed-case\">ECP<\/jats:styled-content>, 17.7\u00a0mg\/L (14.8, 21.1) vs 12.8\u00a0mg\/L (10.9, 14.9) (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.01), and periostin, 73.7 (67.5, 80.3) ng\/<jats:styled-content style=\"fixed-case\">mL<\/jats:styled-content> vs 59.9 (55.8, 64.2) ng\/<jats:styled-content style=\"fixed-case\">mL<\/jats:styled-content> (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.003), than non\u2010sensitized subjects. Periostin levels in this group were also significantly higher than in the group sensitized only to airborne allergens (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.01). Sensitization to food allergens related independently to Fe<jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content> (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.02), S\u2010<jats:styled-content style=\"fixed-case\">ECP<\/jats:styled-content> (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.006) and periostin (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.004), whereas sensitization only to airborne allergens related only to Fe<jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content> (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.02) after adjustments for age, sex, height, weight and smoking history. Fe<jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content> correlated weakly with S\u2010<jats:styled-content style=\"fixed-case\">ECP<\/jats:styled-content> (<jats:italic>r<\/jats:italic>\u00a0=\u00a0.17, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a0.001), periostin (<jats:italic>r<\/jats:italic>\u00a0=\u00a0.19, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a0.001) and U\u2010<jats:styled-content style=\"fixed-case\">EDN<\/jats:styled-content> (0.16, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a0.001). S\u2010<jats:styled-content style=\"fixed-case\">ECP<\/jats:styled-content> also correlated weakly with U\u2010<jats:styled-content style=\"fixed-case\">EDN<\/jats:styled-content> (<jats:italic>r<\/jats:italic>\u00a0=\u00a0.12, <jats:italic>P<\/jats:italic>\u00a0=\u00a0.02). None of the correlations between the remaining pairs of markers of type 2 inflammation were significant.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions &amp; Clinical Relevance<\/jats:title><jats:p>Sensitization to food allergens related to several local and systemic type 2 inflammation markers, such as Fe<jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content>, S\u2010<jats:styled-content style=\"fixed-case\">ECP<\/jats:styled-content> and periostin. Assessing the profile of allergic sensitization, including to food allergens, might improve the understanding and interpretation of inflammatory markers and potentially improve asthma management.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cea.13165","type":"journal-article","created":{"date-parts":[[2018,5,10]],"date-time":"2018-05-10T13:10:31Z","timestamp":1525957831000},"page":"1147-1154","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["IgE sensitization to food allergens and airborne allergens in relation to biomarkers of type 2 inflammation in asthma"],"prefix":"10.1111","volume":"48","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7837-1862","authenticated-orcid":false,"given":"A.","family":"Patelis","sequence":"first","affiliation":[{"name":"Department of Medical Sciences, Respiratory Allergy and Sleep Research Uppsala University Uppsala Sweden"},{"name":"Department of Medical Sciences Clinical Physiology Uppsala University Uppsala Sweden"},{"name":"Division of Medicine Department of Public Health and Clinical Medicine Ume\u00e5 University Ume\u00e5 Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Alving","sequence":"additional","affiliation":[{"name":"Women's and Children's Health Uppsala University Uppsala Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R.","family":"Middelveld","sequence":"additional","affiliation":[{"name":"Institute of Environmental Medicine Karolinska Institute Stockholm Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"James","sequence":"additional","affiliation":[{"name":"Experimental Asthma and Allergy Research National Institute of Enviromental Medicine Karolinska Institutet Stockholm Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"Ono","sequence":"additional","affiliation":[{"name":"Shino\u2010Test Corporation Kanagawa Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Ohta","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine Saga Medical School Saga Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Izuhara","sequence":"additional","affiliation":[{"name":"Division of Medical Biochemistry Department of Biomolecular Sciences Saga Medical School Saga Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. 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