{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T13:25:57Z","timestamp":1790256357457,"version":"4.1.0"},"reference-count":42,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2015,4,24]],"date-time":"2015-04-24T00:00:00Z","timestamp":1429833600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Allergy"],"published-print":{"date-parts":[[2015,8]]},"abstract":"Abstract<\/jats:title>\n \n Background<\/jats:title>\n Asthma and other Th2 inflammatory conditions have been associated with increased susceptibility to viral infections. The mechanisms by which Th2 cytokines can influence immune responses to infections are largely unknown.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n We measured the effects of Th2 cytokines (\n IL<\/jats:styled-content>\n \u20104 and\n IL<\/jats:styled-content>\n \u201013) on bronchial epithelial cell innate immune antiviral responses by assessing interferon (\n IFN<\/jats:styled-content>\n \u2010\u03b2 and\n IFN<\/jats:styled-content>\n \u2010\u03bb1) induction following rhinovirus (\n RV<\/jats:styled-content>\n )\u201016 infection. We also investigated the modulatory effects of Th2 cytokines on Toll\u2010like receptor 3 (\n TLR<\/jats:styled-content>\n 3), interferon\u2010responsive factor 3 (\n IRF<\/jats:styled-content>\n 3) and nuclear factor (\n NF<\/jats:styled-content>\n )\u2010\n kB<\/jats:styled-content>\n , that is key molecules and transcription factors involved in the rhinovirus\u2010induced interferon production and inflammatory cascade. Pharmacological and redox modulation of these pathways was also assessed.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Th2 cytokines impaired\n RV<\/jats:styled-content>\n \u201016\u2010induced interferon production, increased rhinovirus replication and impaired\n TLR<\/jats:styled-content>\n 3 expression in bronchial epithelial cells. These results were replicated\n in\u00a0vivo<\/jats:italic>\n : we found increased\n IL<\/jats:styled-content>\n \u20104\n mRNA<\/jats:styled-content>\n levels in nasal epithelial cells from nasal brushing of atopic rhinitis patients and a parallel reduction in\n TLR<\/jats:styled-content>\n 3 expression and increased\n RV<\/jats:styled-content>\n \u201016 replication compared to nonatopic subjects. Mechanistically, Th2 cytokines impaired\n RV<\/jats:styled-content>\n \u201016\u2010induced activation of\n IRF<\/jats:styled-content>\n 3, but had no effects on\n RV<\/jats:styled-content>\n \u201016\u2010induced\n NF<\/jats:styled-content>\n \u2010\n kB<\/jats:styled-content>\n activation in bronchial epithelial cell cultures. N\u2010acetylcysteine and phosphoinositide 3\u2010kinase (\n PI<\/jats:styled-content>\n 3K) inhibitor restored the inhibitory effects of Th2 cytokines over\n RV<\/jats:styled-content>\n \u201016\u2010induced activation of\n IRF<\/jats:styled-content>\n 3.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n IL<\/jats:styled-content>\n \u20104 and\n IL<\/jats:styled-content>\n \u201013, through inhibition of\n TLR<\/jats:styled-content>\n 3 expression and signalling (\n IRF<\/jats:styled-content>\n 3), impair immune response to\n RV<\/jats:styled-content>\n \u201016 infection. These data suggest that Th2 conditions increase susceptibility to infections and identify pharmacological approaches with potential to restore impaired immune response in these conditions.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/all.12627","type":"journal-article","created":{"date-parts":[[2015,4,8]],"date-time":"2015-04-08T23:03:42Z","timestamp":1428534222000},"page":"910-920","source":"Crossref","is-referenced-by-count":157,"title":["Th2 cytokines impair innate immune responses to rhinovirus in respiratory epithelial cells"],"prefix":"10.1111","volume":"70","author":[{"given":"M.","family":"Contoli","sequence":"first","affiliation":[{"name":"Research Centre on Asthma and COPD Department of Medical Sciences University of Ferrara Ferrara Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K.","family":"Ito","sequence":"additional","affiliation":[{"name":"Airway Disease National Heath and Lung Institute Imperial College London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Padovani","sequence":"additional","affiliation":[{"name":"Research Centre on Asthma and COPD Department of Medical Sciences University of Ferrara Ferrara Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D.","family":"Poletti","sequence":"additional","affiliation":[{"name":"ENT Unit Department of Biomedical and Surgical Sciences University of Ferrara Ferrara Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B.","family":"Marku","sequence":"additional","affiliation":[{"name":"Research Centre on Asthma and COPD Department of Medical Sciences University of Ferrara Ferrara Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. R.","family":"Edwards","sequence":"additional","affiliation":[{"name":"Airway Disease Infection Section National Heart and Lung Institute Imperial College and MRC and Asthma UK Centre in Allergic Mechanisms of Asthma London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L. A.","family":"Stanciu","sequence":"additional","affiliation":[{"name":"Airway Disease Infection Section National Heart and Lung Institute Imperial College and MRC and Asthma UK Centre in Allergic Mechanisms of Asthma London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G.","family":"Gnesini","sequence":"additional","affiliation":[{"name":"Research Centre on Asthma and COPD Department of Medical Sciences University of Ferrara Ferrara Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Pastore","sequence":"additional","affiliation":[{"name":"ENT Unit Department of Biomedical and Surgical Sciences University of Ferrara Ferrara Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Spanevello","sequence":"additional","affiliation":[{"name":"University of Insubria and Fondazione Maugeri Varese Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.","family":"Morelli","sequence":"additional","affiliation":[{"name":"Cros NT Verona Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. L.","family":"Johnston","sequence":"additional","affiliation":[{"name":"Airway Disease Infection Section National Heart and Lung Institute Imperial College and MRC and Asthma UK Centre in Allergic Mechanisms of Asthma London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G.","family":"Caramori","sequence":"additional","affiliation":[{"name":"Research Centre on Asthma and COPD Department of Medical Sciences University of Ferrara Ferrara Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Papi","sequence":"additional","affiliation":[{"name":"Research Centre on Asthma and COPD Department of Medical Sciences University of Ferrara Ferrara Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2015,4,24]]},"reference":[{"key":"e_1_2_7_2_1","unstructured":"Global Initiative for Asthma Global Strategy for Asthma Management and Prevention 2014. 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