{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T05:06:35Z","timestamp":1782968795767,"version":"3.54.5"},"reference-count":34,"publisher":"S. Karger AG","issue":"3","license":[{"start":{"date-parts":[[2021,7,28]],"date-time":"2021-07-28T00:00:00Z","timestamp":1627430400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2021,7,28]],"date-time":"2021-07-28T00:00:00Z","timestamp":1627430400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Innate Immun"],"published-print":{"date-parts":[[2022]]},"abstract":"<jats:p>Asthma exacerbations are commonly triggered by rhinovirus infections. Viruses can activate the NF\u03baB pathway resulting in airway inflammation and increased Th2 cytokine expression. NF\u03baB signaling is also involved in early activation of IFN\u03b2, which is a central mediator of antiviral responses to rhinovirus infection. Using a mouse model, this study tests our hypothesis that NF\u03baB signaling is involved in impaired IFN\u03b2 production at viral-induced asthma exacerbations. C57BL\/6 wild-type and NF\u03baB1&lt;sup&gt;\u2212\/\u2212&lt;\/sup&gt; mice were challenged with house dust mite for 3 weeks and were subsequently stimulated with the rhinoviral mimic poly(I:C). General lung inflammatory parameters and levels of the Th2 upstream cytokine IL-33 were measured after allergen challenge. At exacerbation, production of IFN\u03b2 and antiviral proteins as well as gene expression of pattern recognition receptors and IRF3\/IRF7 was assessed. In the asthma exacerbation mouse model, lack of NF\u03baB1 resulted in lower levels of IL-33 after allergen challenge alone and was associated with reduced eosinophilia. At exacerbation, mice deficient in NF\u03baB1 exhibited enhanced expression of IFN\u03b2 and antiviral proteins. This was accompanied by increased IRF3\/IRF7 expression and induction of pattern recognition receptor expression. In a human asthma dataset, a negative correlation between IRF3 and NF\u03baB1 expression was observed. NF\u03baB may impair antiviral responses at exacerbation, possibly by reducing expression of the transcription factors IRF3\/IRF7. These findings suggest a therapeutic potential for targeting NF\u03baB pathways at viral infection-induced exacerbations. <\/jats:p>","DOI":"10.1159\/000517847","type":"journal-article","created":{"date-parts":[[2021,7,28]],"date-time":"2021-07-28T21:01:47Z","timestamp":1627506107000},"page":"182-191","source":"Crossref","is-referenced-by-count":10,"title":["NF\u03baB1 Dichotomously Regulates Pro-Inflammatory and Antiviral Responses in Asthma"],"prefix":"10.1159","volume":"14","author":[{"given":"Mandy","family":"Menzel","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hamid","family":"Akbarshahi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irma","family":"Mahmutovic 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