{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T17:05:30Z","timestamp":1761843930390},"reference-count":40,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2009,11,25]],"date-time":"2009-11-25T00:00:00Z","timestamp":1259107200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2010,3]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:bold>Background\n\t\t\t\t\t<\/jats:bold> Allergic rhinitis (AR) and asthma often coexist and are referred to as \u2018united airways\u2019 disease. However, the molecular and cellular pathways that are crucially involved in the interaction between upper and lower airways remain to be identified.<\/jats:p><jats:p><jats:bold>Objective\n\t\t\t\t\t<\/jats:bold> We sought to assess whether and how AR exacerbates lower airway inflammation upon allergen challenge in mice.<\/jats:p><jats:p><jats:bold>Methods\n\t\t\t\t\t<\/jats:bold> We previously developed an intranasal ovalbumin (OVA)\u2010driven AR model, characterized by nasal eosinophilic inflammation, enhanced serum levels of OVA\u2010specific IgE and Th2 cytokine production in cervical lymph nodes. In OVA\u2010sensitized mice with or without AR, a lower airway challenge was given, and after 24\u2003h, lower airway inflammation was analysed.<\/jats:p><jats:p><jats:bold>Results\n\t\t\t\t\t<\/jats:bold> We found that AR mice were more susceptible to eosinophilic inflammation following a lower airway OVA challenge than OVA\u2010sensitized controls. AR mice manifested increased numbers of eosinophils in bronchoalveolar lavage fluid and increased inter\u2010cellular adhesion molecule\u20101 (ICAM\u20101) expression on lung endothelium, when compared with OVA\u2010sensitized controls. Depletion of T cells in OVA\u2010challenged AR mice completely abrogated all hallmarks of lower airway inflammation, including enhanced IL\u20105 and tissue eosinophilia. Conversely, adoptive transfer of Th2 effector cells in na\u00efve animals induced lower airway eosinophilic inflammation after challenge with OVA. Blocking T cell recirculation during AR development by the spingosine\u20101 analogue FTY720 also prevented lower airway inflammation including ICAM\u20101 expression in AR mice upon a single lower airway challenge.<\/jats:p><jats:p><jats:bold>Conclusion\n\t\t\t\t\t<\/jats:bold> Our mouse model of \u2018united airways\u2019 disease supports epidemiological and clinical data that AR has a significant impact on lower airway inflammation. Circulating Th2 effector cells are responsible for lung priming in AR mice, most likely through up\u2010regulation of ICAM\u20101.<\/jats:p><jats:p> <jats:italic>Cite this as<\/jats:italic>: A. KleinJan, M. Willart, M. van Nimwegen, K. Leman, H. C. Hoogsteden, R.W. Hendriks and B.N. Lambrecht, <jats:italic>Clinical &amp; Experimental Allergy<\/jats:italic>, 2010 (40) 494\u2013504.<\/jats:p>","DOI":"10.1111\/j.1365-2222.2009.03417.x","type":"journal-article","created":{"date-parts":[[2009,11,26]],"date-time":"2009-11-26T06:44:24Z","timestamp":1259217864000},"page":"494-504","source":"Crossref","is-referenced-by-count":32,"title":["United airways: circulating Th2 effector cells in an allergic rhinitis model are responsible for promoting lower airways inflammation"],"prefix":"10.1111","volume":"40","author":[{"given":"A.","family":"KleinJan","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Willart","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Van Nimwegen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Leman","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H. 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