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PMID: 15276138 Published · ppublish English Journal Article Review

Mechanisms of rhinovirus-induced asthma.

Paediatric respiratory reviews ·Vol. 5 ·No. 3 ·2004-09-00 ·Pages 255-60

Papadopoulos NG, Papi A, Psarras S, Johnston SL

Abstract

Several epidemiological studies using sensitive detection methodologies have confirmed that the majority of acute asthma exacerbations follow upper respiratory tract infections--common colds. Most of these colds are due to human rhinoviruses (RVs). RVs are able to reach and replicate in epithelial cells of the lower airways and can activate these cells to produce pro-inflammatory mediators. Under some circumstances, RVs can also become cytotoxic to the epithelium. Atopic asthmatic individuals produce less interferon-gamma and more interleukin-10 than normal subjects in response to RV infection. Symptom severity as well as viral shedding after experimental RV infection, is inversely correlated with 'atopic' status, expressed as the interferon-gamma to interleukin-5 ratio. Expression of co-stimulatory molecules on immune cells is also affected in atopic asthmatics, suggesting an aberrant immune response to RV that may lead to suboptimal viral clearance and viral persistence. Some of the above effects can be reversed in vitro by corticosteroids, second-generation antihistamines or anti-oxidants; however, the optimal strategy for treating acute asthma exacerbations requires further research at both mechanistic and clinical levels.

MeSH Terms
Asthma/immunology,virology Common Cold/complications,immunology Humans Rhinovirus/pathogenicity,physiology
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Papadopoulos Nikolaos G
Allergy Department, Second Paediatric Clinic, University of Athens, Greece. ngp@allergy.gr
Papi Alberto
Psarras Stelios
Johnston Sebastian L
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Article Info
Journal
Paediatric respiratory reviews
Abbr.
Paediatr Respir Rev
ISSN
1526-0542
Published
2004-09-00
Pages
255-60
Language
English
Region
England
NLM ID
100898941
PMCID
PMC7172503
Subset
IM
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