Imperial College London
Alternate

ProfessorSebastianJohnston

Faculty of Medicine, National Heart & Lung Institute

Asthma UK Clinical Chair
 
 
 
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Contact

 

+44 (0)7931 376 544s.johnston

 
 
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Assistant

 

Mr Christophe Tytgat +44 (0)20 7594 3849

 
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Location

 

343Norfolk PlaceSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Zhu:2019:10.1016/j.jaci.2018.04.003,
author = {Zhu, J and Message, SD and Mallia, P and Kebadze, T and Contoli, M and Ward, CK and Barnathan, ES and Mascelli, MA and Kon, OM and Papi, A and Stanciu, LA and Edwards, MR and Jeffery, PK and Johnston, SL},
doi = {10.1016/j.jaci.2018.04.003},
journal = {Journal of Allergy and Clinical Immunology},
pages = {114--125.e4},
title = {Bronchial mucosal Interferon-α/β and pattern recognition receptor expression in experimental rhinovirus-induced asthma exacerbations},
url = {http://dx.doi.org/10.1016/j.jaci.2018.04.003},
volume = {143},
year = {2019}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - BACKGROUND: The innate immune system senses viral infection via pattern recognition receptors (PRRs) leading to type I interferon (IFN) production: their roles in rhinovirus (RV)-induced asthma exacerbations in vivo are uncertain. OBJECTIVES: To compare bronchial mucosal type I IFN and PRR expression at baseline and following RV infection in atopic asthmatic and control subjects. METHODS: Immunohistochemistry was used to detect expression of IFN-α, IFN-β and the PRRs, toll-like receptor (TLR)-3, melanoma-differentiation-associated gene-5 (MDA-5) and retinoic-acid-inducible protein-I (RIG-I) in bronchial biopsies from 10 atopic asthmatics and 15 non-asthmatic non-atopic controls at baseline and on day four and six weeks following RV infection. RESULTS: We observed IFN-α/β deficiency in bronchial epithelium at three time points in asthma in vivo. Lower epithelial IFN-α/β expression was related to greater virus load, worse airway symptoms, airway hyperresponsiveness (AHR) and reductions in lung function during RV infection. We found lower frequencies of bronchial subepithelial monocytes/macrophages expressing IFN-α/β in asthma during infection. IFN deficiency at baseline was not accompanied by deficient PRR expression in asthma. Both epithelial and subepithelial PRR expression was induced during RV infection. RV infection increased numbers of subepithelial IFN/PRRs-expressing inflammatory cells were related to greater virus load, AHR and reductions in lung function. CONCLUSIONS: Bronchial epithelial IFN-α/β expression and numbers of subepithelial IFN-α/β-expressing monocytes/macrophages during infection were both deficient in asthma. Lower epithelial IFN-α/β expression was associated with adverse clinical outcomes following RV infection in vivo. Increases in subepithelial cells expressing IFN/PRRs during infection were also related to greater virus load/illness severity.
AU  - Zhu,J
AU  - Message,SD
AU  - Mallia,P
AU  - Kebadze,T
AU  - Contoli,M
AU  - Ward,CK
AU  - Barnathan,ES
AU  - Mascelli,MA
AU  - Kon,OM
AU  - Papi,A
AU  - Stanciu,LA
AU  - Edwards,MR
AU  - Jeffery,PK
AU  - Johnston,SL
DO  - 10.1016/j.jaci.2018.04.003
EP  - 125
PY  - 2019///
SN  - 0091-6749
SP  - 114
TI  - Bronchial mucosal Interferon-α/β and pattern recognition receptor expression in experimental rhinovirus-induced asthma exacerbations
T2  - Journal of Allergy and Clinical Immunology
UR  - http://dx.doi.org/10.1016/j.jaci.2018.04.003
UR  - https://www.ncbi.nlm.nih.gov/pubmed/29698627
UR  - http://hdl.handle.net/10044/1/58898
VL  - 143
ER  -
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