Published ahead of print on August 19, 2003, doi:10.1164/rccm.200306-737OC
Am. J. Respir. Crit. Care Med., Volume 168, Number 9, November 2003, 1091-1094
A more recent version of this article appeared on November 1, 2003
Submitted on June 4, 2003
Accepted on August 18, 2003
Rhinovirus-induced Interferon Gamma and Airway Responsiveness in Asthma
G. Daniel Brooks1*, Kim A Buchta1, Cheri A Swenson1, James E Gern2, and William W Busse1
1 Medicine, University of Wisconsin, Madison, WI, USA,
2 Pediatrics, University of Wisconsin, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: gdb{at}medicine.wisc.edu.
The majority of asthma exacerbations are caused by respiratory infections, with rhinovirus being the most common virus. Recent evidence has suggested that decreased generation of interferon gamma (IFN ) is associated with more severe colds and delayed elimination of virus. Whether the generation of IFN also has any relationship to general features of asthma severity has yet to be determined. To evaluate this hypothesis, peripheral blood mononuclear cells from 19 atopic asthmatic subjects were incubated with rhinovirus 16 for six days to determine IFN and interleukin-5 (IL-5) production; these responses were then compared to measurements of airflow obstruction and airway responsiveness. Rhinovirus 16-induced IFN production correlated significantly with the methacholine provocative dose (r = 0.50, p = 0.03), and the ratio of rhinovirus 16-induced IFN/IL-5 correlated with percent predicted FEV1 (r = 0.53, p = 0.02). In contrast, there were no significant associations between measures of asthma severity and rhinovirus-induced IL-5. These findings suggest that a cytokine imbalance with a deficient T helper, type 1 response to rhinovirus, but not a T helper, type 2 response, is associated with measures of asthma severity and support the concept that impaired antiviral responses may be associated with asthma severity.
Key words: Asthma, Rhinovirus, Viruses, Interferon Type II
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