RT Journal Article SR Electronic T1 Nasal upregulation of CST1 in dog sensitised children with severe allergic airway disease JF ERJ Open Research JO erjor FD European Respiratory Society SP 00917-2020 DO 10.1183/23120541.00917-2020 A1 Käck, Ulrika A1 Einarsdottir, Elisabet A1 van Hage, Marianne A1 Asarnoj, Anna A1 James, Anna A1 Nopp, Anna A1 Krjutskov, Kaarel A1 Katayama, Shintaro A1 Kere, Juha A1 Lilja, Gunnar A1 Söderhäll, Cilla A1 Konradsen, Jon R. YR 2021 UL http://openres.ersjournals.com/content/early/2021/02/04/23120541.00917-2020.abstract AB Background The clinical presentation of children sensitised to dog dander varies from asymptomatic to severe allergic airway disease, but the genetic mechanisms underlying these differences are not clear.Objective To investigate nasal transcriptomic profiles associated with dog dander sensitisation in school children and to reveal clinical symptoms related with these profiles.Methods RNA was extracted from nasal epithelial cell brushings of children sensitised to dog dander and healthy controls. Blood sample analyses included IgE against dog dander, dog allergen molecules, other airborne and food allergens, basophil activation and white blood cell counts. Clinical history of asthma and rhinitis was recorded, and lung function was assessed (spirometry, methacholine provocation and FeNO).Results The most over-expressed gene in children sensitised to dog dander compared to healthy controls was CST1, coding for Cystatin 1. A cluster of these children with enhanced CST1 expression showed lower FEV1, increased bronchial hyper-reactivity, pronounced eosinophilia and higher basophil allergen threshold sensitivity compared with other children sensitised to dog dander. Multi-sensitisation to lipocalins was also more common in this group.Conclusions Over-expression of CST1 is associated with more severe allergic airway disease in children sensitised to dog dander. CST1 is thus a possible biomarker of the severity of allergic airway disease and a possible therapeutic target for the future treatment of airborne allergy.FootnotesThis manuscript has recently been accepted for publication in the ERJ Open Research. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJOR online. Please open or download the PDF to view this article.Conflict of interest: U. Käck reports a lecture fee from Thermo Fisher outside the submitted work.Conflict of interest: Dr. Einarsdottir has nothing to disclose.Conflict of interest: M. van Hage reports lecture fees from Thermo Fisher Scientific and ALK, and consultancy fees from Biomay AG, Vienna, Austria and Hycor Biomedical LLC, CA, US, outside the submitted work.Conflict of interest: Dr. Asarnoj has nothing to disclose.Conflict of interest: Dr. James has nothing to disclose.Conflict of interest: Dr. Nopp has nothing to disclose.Conflict of interest: Dr. Krjutškov has nothing to disclose.Conflict of interest: Dr. Katayama reports grants from Jane and Aatos Erkko Foundation, during the conduct of the study.Conflict of interest: Dr. Kere has nothing to disclose.Conflict of interest: Dr. Lilja has nothing to disclose.Conflict of interest: Dr. Söderhäll has nothing to disclose.Conflict of interest: Dr. Konradsen has received material from Thermo Fishes Scientific to perform IgE analysis in this project.