Volume 124, Issue 2 , Pages 245-252.e3, August 2009
Similar colds in subjects with allergic asthma and nonatopic subjects after inoculation with rhinovirus-16
Background
Rhinovirus infections are frequent causes of asthma exacerbations.
Objective
This study was conducted to test whether subjects with and without allergic asthma have different responses to infection and to identify baseline patient risk factors that predict cold outcomes.
Methods
Twenty subjects with mild persistent allergic asthma and 18 healthy subjects were experimentally inoculated with rhinovirus-16. Subjects were evaluated at baseline, during the acute infection, and during recovery for asthma and cold symptoms by using a validated questionnaire. Sputum and nasal lavage fluid were evaluated for viral shedding, cytokines, and cellular inflammation.
Results
There were no group-specific significant differences in peak cold symptom scores (10.0 ± 5.8 vs 11.1 ± 6.2, asthmatic vs healthy subjects), peak nasal viral titers (log10 4.3 ± 0.8 vs 3.7 ± 1.4 50% tissue culture infective dose/mL, respectively), or changes in peak flow during the study (10% ± 10% vs 8% ± 6%, respectively). Rhinovirus-16 infection increased peak asthma index values in the asthmatic group (median, 6 → 13; P = .003) but only marginally in the healthy group (median, 4 → 7; P = .09). More asthmatic subjects had detectable eosinophils in nasal lavage and sputum samples at baseline and during infection, but otherwise, cellular and cytokine responses were similar. Baseline sputum eosinophilia and CXCL8 (IL-8) levels were positively associated with cold symptoms, whereas CCL2 (monocyte chemotactic protein 1) levels were inversely associated with nasal viral shedding.
Conclusions
These findings suggest that subjects with mild allergic asthma and healthy subjects have similar cold symptoms and inflammatory and antiviral responses. In addition, eosinophilia and other selective baseline measures of airway inflammation in subjects with or without asthma might predict respiratory outcomes with rhinovirus infection.
Key words: Asthma, viral respiratory tract infections, virus-induced asthma, rhinovirus, eosinophil, CCL2, CXCL8, total serum IgE, allergy, common cold
Abbreviations used: PEF, Peak expiratory flow, PFU, Plaque-forming units, RV16, Rhinovirus-16, TCID50, 50% Tissue culture infective dose, TDHSS, Total daily highest symptom score
Supported by funds from National Institutes of Health and National Institute of Allergy and Infectious Diseases grants P01 AI50500 and U19 AI070503-01.
Disclosure of potential conflict of interest: R. Sorkness receives research support from the National Institutes of Health and Modus Biological Membranes. W. W. Busse is on the advisory board/a consultant for Genentech/Novartis, Altair, GlaxoSmithKline, Altana, Wyeth, Pfizer, Dynavax, Centocor, and Schering-Plough; is a speaker for GlaxoSmithKline, Novartis, Merck, and AstraZeneca; and received research support from Novartis, Dynavax, Wyeth, Centocor, and GlaxoSmithKline. The rest of the authors have declared that they have no conflict of interest.
PII: S0091-6749(09)00854-9
doi:10.1016/j.jaci.2009.05.030
© 2009 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
Volume 124, Issue 2 , Pages 245-252.e3, August 2009
