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{Johnston:2007:10.1513/pats.200701-030AW,
author = {Johnston, SL},
doi = {10.1513/pats.200701-030AW},
journal = {Proc Am Thorac Soc},
pages = {267--270},
title = {Innate immunity in the pathogenesis of virus-induced asthma exacerbations.},
url = {http://dx.doi.org/10.1513/pats.200701-030AW},
volume = {4},
year = {2007}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - The major asthma morbidity, mortality, and health care costs are a result of acute exacerbations. However, exacerbations are only partially responsive to current therapies and new approaches to treatment are needed. The great majority of acute asthma exacerbations are associated with respiratory viral infections and, of viruses implicated, approximately 60% are human rhinoviruses (RVs). The mechanisms of RV-induced asthma exacerbations are poorly understood. We have previously shown that adults with asthma have increased susceptibility to naturally occurring RV infections. Our recent studies have investigated mechanisms of innate host defense against RV infection. First, primary bronchial epithelial cells from subjects with asthma were shown to replicate RV in vitro to several logs, whereas those of normal control subjects were resistant to infection. This resistance was a result of rapid induction of apoptosis and of interferon (IFN)-beta in the normal cells, whereas these responses were deficient in asthmatic cells. These studies were recently extended to a novel family of three related proteins, the IFN-lambdas 1-3, production of which was also deficient in vitro and related to asthma exacerbation severity in vivo. These studies identify novel mechanisms for the increased susceptibility of subjects with asthma to RV infection. Further studies are now required to investigate whether administration of IFN-beta or IFN-lambda may be beneficial in the treatment of asthma exacerbations, to determine whether similar deficiencies are observed in children and in subjects with nonatopic asthma, and to investigate the mechanisms of deficient IFN production in asthma to help identify better therapeutic strategies for asthma exacerbations.
AU  - Johnston,SL
DO  - 10.1513/pats.200701-030AW
EP  - 270
PY  - 2007///
SN  - 1546-3222
SP  - 267
TI  - Innate immunity in the pathogenesis of virus-induced asthma exacerbations.
T2  - Proc Am Thorac Soc
UR  - http://dx.doi.org/10.1513/pats.200701-030AW
UR  - https://www.ncbi.nlm.nih.gov/pubmed/17607011
VL  - 4
ER  -
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