Imperial College London
Alternate

DrNathanBartlett

Faculty of Medicine, National Heart & Lung Institute

Honorary Senior Lecturer
 
 
 
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Contact

 

n.bartlett

 
 
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Location

 

Wright Fleming WingSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Beale:2014:10.1126/scitranslmed.3009124,
author = {Beale, J and Jayaraman, A and Jackson, DJ and Macintyre, JDR and Edwards, MR and Walton, RP and Zhu, J and Ching, YM and Shamji, B and Edwards, M and Westwick, J and Cousins, DJ and Hwang, YY and McKenzie, A and Johnston, SL and Bartlett, NW},
doi = {10.1126/scitranslmed.3009124},
journal = {Science Translational Medicine},
title = {Rhinovirus-induced IL-25 in asthma exacerbation drives type 2 immunity and allergic pulmonary inflammation},
url = {http://dx.doi.org/10.1126/scitranslmed.3009124},
volume = {6},
year = {2014}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - 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.
AU  - Beale,J
AU  - Jayaraman,A
AU  - Jackson,DJ
AU  - Macintyre,JDR
AU  - Edwards,MR
AU  - Walton,RP
AU  - Zhu,J
AU  - Ching,YM
AU  - Shamji,B
AU  - Edwards,M
AU  - Westwick,J
AU  - Cousins,DJ
AU  - Hwang,YY
AU  - McKenzie,A
AU  - Johnston,SL
AU  - Bartlett,NW
DO  - 10.1126/scitranslmed.3009124
PY  - 2014///
SN  - 1946-6234
TI  - Rhinovirus-induced IL-25 in asthma exacerbation drives type 2 immunity and allergic pulmonary inflammation
T2  - Science Translational Medicine
UR  - http://dx.doi.org/10.1126/scitranslmed.3009124
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000343317700004&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
VL  - 6
ER  -
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