Background: Despite the strong association of asthma exacerbations with rhi
novirus (RV) infection, inoculation of asthmatic subjects with RV only caus
es small changes in loner airway function, suggesting that RV infection is
not itself sufficient to provoke asthma exacerbations.
Objective: Our purpose was to test whether allergic inflammation increases
the airway response to RV infection.
Methods: We compared the severity of RV type 16-induced colds in 2 groups o
f 10 subjects with allergic rhinitis. One group received 3 nasal challenges
with allergen and the other received challenges with placebo over the week
before nasal inoculation with RV type 16 (4000 tissue culture infective do
se 50% per subject). Subjects kept symptom diaries and were assessed with s
pirometry, methacholine challenge, nasal lavage, and sputum induction on da
ys 2, 4, 7, 10, 15, and 30 after inoculation.
Results: The 2 groups developed equal rates of infection (90%), similar col
d symptoms (Jackson score median [interquartile range], 11 [6-33] vs 20.5 [
6-42] for allergen and placebo groups respectively, P = .54), and similar c
hanges in cellular profile and in IL-6 and IL-8 concentrations in nasal lav
age fluid and induced sputum after RV inoculation. The incubation period wa
s significantly longer in the allergen group (2.5 [1-5.5] vs 1 [1-1] day, P
= .03) and the duration of cold symptoms was shorter (5 [4.7] vs 8.5 [6-10
] days, P = .008). We also found an inverse correlation between the percent
of eosinophils in nasal lavage fluid before inoculation and the severity o
f cold symptoms (r = -0.58, P = .008).
Conclusion: In subjects with allergic rhinitis, augmented nasal allergic in
flammation before inoculation with RV type 16 does not worsen the severity
of cold symptoms but delays their onset and shortens their duration.