Airway
inflammation in
asthma may represent a favorable environment for respiratory
viral infections, augmenting virus-induced exacerbations in
asthma. We postulated that repeated low-dose
allergen exposure preceding experimental rhinovirus 16 (RV16)
infection increases the severity of RV-induced
airway obstruction and
inflammation. Thirty-six house dust mite-allergic patients with mild to moderate
asthma participated in a three-arm, parallel, placebo-controlled, double-blind study. Patients inhaled a low dose of house dust mite
allergen for 10 subsequent working days (Days 1-5 and 8-12) and/or were subsequently infected with RV16 (Days 15 and 16).
Allergen exposure resulted in a significant fall in FEV1 (p < 0.001) and provocative concentration of
histamine causing a 20% fall in FEV1 (p < 0.001) and an increase in exhaled
nitric oxide (p < 0.001) and percentage of sputum eosinophils (p < 0.001). RV16
infection led to a fall in FEV1 (p = 0.02) and increases in the percentage of sputum neutrophils (p = 0.01), sputum
interleukin-8 (p = 0.04), and
neutrophil elastase (p = 0.04). Successive
allergen exposure and RV16
infection had no synergistic or additive effect on any of the clinical or inflammatory outcomes. In conclusion, repeated low-dose
allergen exposure and RV16
infection induce distinct inflammatory profiles within the airways in
asthma without apparent interaction between these two environmental triggers. This suggests that preceding
allergen exposure, at the used dose and duration, is not a determinant of the severity of RV-induced exacerbations in patients with mild to moderate
asthma.