- Handzel ZT,
- Busse WW,
- Sedgwick JB,
- et al.
Infection with rhinovirus (RV) is a potent trigger for the exacerbation of asthma. RV may act to augment allergic inflammation in the lung, especially eosinophilic inflammation.
Eosinophils (EOS) were recovered from 13 allergic rhinitis and 8 atopic asthmatic subjects. All subjects were skin test positive.
Radiolabeled RV 16 did not bind to isolated EOS. When EOS were first stimulated with granulocyte-macrophage colony-stimulating factor (GM-CSF), which upregulates ICAM-1 (a surface marker) on EOS, RV was bound to EOS. This could be blocked with anti-ICAM. RV alone did not increase ICAM expression on EOS. T-cells previously sensitized to RV were stimulated to proliferate when further exposed to the EOS with bound RV, and these T-cells produced large amounts of interferon-gamma.
Eosinophils may contribute to asthma exacerbations by acting as antigen presenting cells to T-cells, which activate antiviral processes that increase lung inflammation, a detriment to asthmatics.
Viral illnesses account for most acute exacerbations of asthma in children. RVs are the most common viruses implicated. Effective strategies to reduce the consequences of viral-induced pulmonary inflammation in asthma would have a great impact on asthma care.