Background: Hyper-responsiveness of nasal secretory function and volume changes are features of allergic rhinitis (AR) that are mediated in part by neural mechanisms. The finding of nasal hyper-responsiveness in subjects with AR who are currently symptomatic, but not in those who are currently out of season and asymptomatic, suggests that induction of neural reflexes in allergic subjects occurs as a result of allergic inflammation.
Objectives: To investigate whether allergen exposure in subjects with asymptomatic seasonal allergic rhinitis (SAR) may lead to induction of neural reflexes, and to investigate the components of the reflexes involved in this induction.
Methods: Asymptomatic subjects with (out-of-season) SAR underwent a nasal bradykinin challenge, before and 24 h after preceding ipsilateral (n = 11) and contralateral (n = 11) antigen challenge. Challenges were performed and nasal secretions collected using filter paper disks, and changes in nasal minimal cross-sectional area (A(min)) were measured using acoustic rhinometry.
Results: Preceding ipsilateral antigen challenge led to the induction of a contralateral secretory reflex (P = 0.01), which was absent in control experiments (P = 0.34). Ipsilateral secretion weights were also enhanced. Preceding contralateral antigen challenge also induced a contralateral secretory reflex (P = 0.03). Enhancement of the reduction in contralateral A(min) was also seen (P = 0.02). Ipsilateral responses were unchanged.
Conclusions: Allergen exposure in asymptomatic allergic subjects leads to induction of neural reflexes, resulting in nasal hyper-responsiveness, which persists beyond the resolution of the acute allergic response. Our data suggest that the mechanisms of allergen-induced hyper-responsiveness involve both afferent and efferent components.