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Published ahead of print on May 13, 2005, doi:10.1164/rccm.200412-1621OC

Am. J. Respir. Crit. Care Med., Volume 172, Number 4, August 2005, 433-439

A more recent version of this article appeared on August 15, 2005
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Submitted on December 2, 2004
Accepted on May 9, 2005

IL-10 Gene Expression in Acute Virus-induced Asthma

Terry V Grissell1, Heather Powell2, Darren R Shafren3, Michael J Boyle4, Michael J Hensley1, Peter D Jones5, Bruce F Whitehead6, and Peter G Gibson1*

1 School of Medical Practice and Population Health, University of Newcastle, Callaghan, NSW, Australia; Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, John Hunter Hospital, New Lambton, NSW, Australia, 2 Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, John Hunter Hospital, New Lambton, NSW, Australia, 3 School of Medical Practice and Population Health, University of Newcastle, Callaghan, NSW, Australia; Picornaviral Research Unit, Royal Newcastle Hospital, Newcastle, NSW, Australia, 4 School of Medical Practice and Population Health, University of Newcastle, Callaghan, NSW, Australia; Immunology and Infectious Diseases Unit, John Hunter Hospital, New Lambton, NSW, Australia, 5 School of Medical Practice and Population Health, University of Newcastle, Callaghan, NSW, Australia, 6 Kaleidoscope, John Hunter Children's Hospital, New Lambton, NSW, Australia

* To whom correspondence should be addressed. E-mail: Peter.Gibson{at}hnehealth.nsw.gov.au.

Rationale: Virus-induced asthma is characterised by a marked neutrophil influx and eosinophil degranulation, suggesting a different immunopathogenesis to allergen-induced asthma. Objectives: This study compared induced sputum cytokine responses in subjects with a severe asthma exacerbation and respiratory virus infection to stable asthma, healthy controls and virus-infected non-asthmatic subjects. Methods: Subject infection status and pulmonary history were established using common cold and asthma questionnaires, and lung function and atopy tests were performed. Respiratory virus infection was diagnosed using cell culture and direct PCR on induced sputum. The induced sputum cellular profile was examined and cytokine gene expression assessed using quantitative real-time PCR. Results: A respiratory virus was detected in 78% of subjects with acute asthma. Specific viruses detected were rhinovirus (83%), influenza (15%), enterovirus (4%) and respiratory syncytial virus (2%). Virus-infected subjects with acute asthma or no asthma had increased RANTES and MIP-1{alpha} messenger RNA compared to other groups. Interleukin-10 mRNA was significantly increased in virus-infected acute asthma and reduced on recovery from acute asthma. Interleukin-5, eotaxin and interleukin-8 mRNA transcripts were similar across groups. Conclusions: Asthma exacerbation triggered by respiratory virus infection is characterised by increased IL-10 gene expression that may explain the suppressed eosinophil influx in acute asthma. Airway neutrophilia due to respiratory virus infection is associated with chemokine gene expression involving RANTES and MIP-1{alpha}.
Key words: Asthma, viruses, gene expression, cytokines




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