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Title: Rhinovirus-induced IL-25 in asthma exacerbation drives type 2 immunity and allergic pulmonary inflammation
Authors: Beale, Janine
Jayaraman, Annabelle
Jackson, David J.
Macintyre, Jonathan D. R.
Edwards, Michael R.
Walton, Ross P.
Zhu, Jie
Ching, Yee Man
Shamji, Betty
Edwards, Matt
Westwick, John
Cousins, David J.
Hwang, You Yi
McKenzie, Andrew
Johnston, Sebastian L.
Bartlett, Nathan W.
First Published: 1-Oct-2014
Publisher: American Association for the Advancement of Science
Citation: Science Translational Medicine, 2014, 6 (265), p. 256ra134
Abstract: Rhinoviruses (RVs), which are the most common cause of virally induced asthma exacerbations, account for much of the burden of asthma in terms of morbidity, mortality, and associated cost. Interleukin-25 (IL-25) activates type 2–driven inflammation and is therefore potentially important in virally induced asthma exacerbations. To investigate this, we examined whether RV-induced IL-25 could contribute to asthma exacerbations. RV-infected cultured asthmatic bronchial epithelial cells exhibited a heightened intrinsic capacity for IL-25 expression, which correlated with donor atopic status. In vivo human IL-25 expression was greater in asthmatics at baseline and during experimental RV infection. In addition, in mice, RV infection induced IL-25 expression and augmented allergen-induced IL-25. Blockade of the IL-25 receptor reduced many RV-induced exacerbation-specific responses including type 2 cytokine expression, mucus production, and recruitment of eosinophils, neutrophils, basophils, and T and non-T type 2 cells. Therefore, asthmatic epithelial cells have an increased intrinsic capacity for expression of a pro–type 2 cytokine in response to a viral infection, and IL-25 is a key mediator of RV-induced exacerbations of pulmonary inflammation.
DOI Link: 10.1126/scitranslmed.3009124
ISSN: 1946-6234
eISSN: 1946-6242)
Version: Post-print
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © 2014, American Association for the Advancement of Science. Deposited with reference to the publisher’s archiving policy available on the SHERPA/RoMEO website.
Description: This is the author’s version of the work. It is posted here by permission of the AAAS for personal use, not for redistribution. The definitive version was published in Science Translational Medicine on 6 (256), DOI: 10.1126/scitranslmed.3009124
Appears in Collections:Published Articles, School of Management

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