Gj. Braunstahl et al., Segmental bronchial provocation induces nasal inflammation in allergic rhinitis patients, AM J R CRIT, 161(6), 2000, pp. 2051-2057
Allergic rhinitis and asthma often coexist and share a genetic background.
Pathophysiologic connections between the nose and lungs are still not entir
ely understood. This study was undertaken to compare allergic inflammation
and clinical findings in the upper and lower airways after segmental bronch
ial provocation (SBP) in nonasthmatic allergic rhinitis patients. Eight non
asthmatic, grass pollen-sensitive patients with allergic rhinitis and eight
healthy controls were included. Bronchial biopsies and blood samples were
taken before (T-0) and 24 h (T-24) after SBP. Nasal biopsies were obtained
at T-0, 1 h after SEP (T-1), and T-24. Immunohistochemical staining was per
formed for eosinophils (BMK13), interleukin (IL)-5, and eotaxin. The number
of eosinophils increased in the challenged and unchallenged bronchial muco
sa (p < 0.05) and in the blood (p = 0.03) of atopic subjects at T-24. We de
tected an increase of BMK13-positive and eotaxin-positive cells in the nasa
l lamina propria and enhanced expression of IL-5 in the nasal epithelium of
atopic subjects only at T-24 (p < 0.05). SEP induced nasal and bronchial s
ymptoms as well as reductions in pulmonary and nasal function in the allerg
ic group. No significant changes could be observed in healthy controls. The
study shows that SEP in nonasthmatic allergic rhinitis patients results in
peripheral blood eosinophilia, and that SEP can induce allergic inflammati
on in the nose.