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However, the role of <jats:styled-content style=\"fixed-case\">CHI<\/jats:styled-content>3L1 in airway inflammation induced by respiratory viruses has not been investigated. The aim of this study was to investigate the relationship between <jats:styled-content style=\"fixed-case\">CHI<\/jats:styled-content>3L1 and airway inflammation caused by respiratory syncytial virus (<jats:styled-content style=\"fixed-case\">RSV<\/jats:styled-content>) infection.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We measured <jats:styled-content style=\"fixed-case\">YKL<\/jats:styled-content>\u201040 levels in human nasopharyngeal aspirate (<jats:styled-content style=\"fixed-case\">NPA<\/jats:styled-content>) from hospitalized children presenting with acute respiratory symptoms. Wild\u2010type (<jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>) and <jats:styled-content style=\"fixed-case\">BRP<\/jats:styled-content>\u201039 knockout (<jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content>) C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/6 mice were inoculated with live <jats:styled-content style=\"fixed-case\">RSV<\/jats:styled-content> (A2 strain). Bronchoalveolar lavage fluid and lung tissue samples were obtained on day 7 after inoculation to assess lung inflammation, airway reactivity, and expression of cytokines and <jats:styled-content style=\"fixed-case\">BRP<\/jats:styled-content>\u201039.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In human subjects, <jats:styled-content style=\"fixed-case\">YKL<\/jats:styled-content>\u201040 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201013 levels in <jats:styled-content style=\"fixed-case\">NPA<\/jats:styled-content> were higher in children with <jats:styled-content style=\"fixed-case\">RSV<\/jats:styled-content> infection than in control subjects. Expression of <jats:styled-content style=\"fixed-case\">BRP<\/jats:styled-content>\u201039 and Th2 cytokines, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201013 in particular, was increased following <jats:styled-content style=\"fixed-case\">RSV<\/jats:styled-content> infection in mice. Airway\u00a0inflammation caused by <jats:styled-content style=\"fixed-case\">RSV<\/jats:styled-content> infection was reduced in <jats:styled-content style=\"fixed-case\">BRP<\/jats:styled-content>\u201039 <jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content> mice as compared to <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice. Th2 cytokine levels were not increased in the lungs of <jats:styled-content style=\"fixed-case\">RSV<\/jats:styled-content>\u2010infected <jats:styled-content style=\"fixed-case\">BRP<\/jats:styled-content>\u201039 <jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content> mice. <jats:styled-content style=\"fixed-case\">BRP<\/jats:styled-content>\u201039 regulated M2 macrophage activation\u00a0in\u00a0<jats:styled-content style=\"fixed-case\">RSV<\/jats:styled-content>\u2010infected mice. Additionally, treatment with anti\u2010<jats:styled-content style=\"fixed-case\">CHI<\/jats:styled-content>3L1 antibody attenuated airway inflammation and Th2 cytokine production in <jats:styled-content style=\"fixed-case\">RSV<\/jats:styled-content>\u2010infected <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These findings suggest that <jats:styled-content style=\"fixed-case\">CHI<\/jats:styled-content>3L1 could contribute to airway inflammation induced by <jats:styled-content style=\"fixed-case\">RSV<\/jats:styled-content> infection. <jats:styled-content style=\"fixed-case\">CHI<\/jats:styled-content>3L1 could be a potential therapeutic\u00a0candidate for attenuating Th2\u2010associated immunopathology during <jats:styled-content style=\"fixed-case\">RSV<\/jats:styled-content> infection.<\/jats:p><\/jats:sec>","DOI":"10.1111\/all.13661","type":"journal-article","created":{"date-parts":[[2018,11,7]],"date-time":"2018-11-07T09:49:52Z","timestamp":1541584192000},"page":"685-697","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":36,"title":["Chitinase 3\u2010like 1 protein plays a critical role in respiratory syncytial virus\u2010induced airway inflammation"],"prefix":"10.1111","volume":"74","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5634-9709","authenticated-orcid":false,"given":"Min Jung","family":"Kim","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology Brain Korea 21 PLUS Project for Medical Science Yonsei University College of Medicine Seoul Korea"},{"name":"Department of Pediatrics Severance Hospital Institute of Allergy Brain Korea 21 PLUS Project for Medical Science Yonsei University College of Medicine Seoul 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