Mm. Riccio et D. Proud, EVIDENCE THAT ENHANCED NASAL REACTIVITY TO BRADYKININ IN PATIENTS WITH SYMPTOMATIC ALLERGY IS MEDIATED BY NEURAL REFLEXES, Journal of allergy and clinical immunology, 97(6), 1996, pp. 1252-1263
Objective: The aim of this study was to determine whether allergic inf
lammation induces nasal hyperreactivity to bradykinin by enhancing neu
ronal responsiveness. Methods: We compared the response to localized,
unilateral nasal challenge with bradykinin in patients with perennial
allergic rhinitis and nonallergic subjects, and in patients with seaso
nal allergic rhinitis challenged in and out of season. Weights of secr
etions from each nostril were recorded, and levels of albumin and lact
oferrin in secretions recovered from each nostril were assayed. Contra
lateral administration of atropine (0.32 mg) was used to evaluated the
role of cholinergic reflexes in nasal hyperresponsiveness to bradykin
in. Results: In patients with symptomatic allergy, bradykinin induced
greater symptoms scores than in asymptomatic atopic or nonallergic con
trol subjects. Moreover, bradykinin caused sneezing in a majority of p
atients with symptomatic allergy but in none of the asymptomatic atopi
c or nonallergic control subjects. Only patients with symptomatic alle
rgy showed dose-dependent bilateral increases in secretion weights and
levels of the serous glandular maker, lactoferrin. In contrast, brady
kinin induced similar increases in ipsilateral, but not contralateral,
levels of albumin in all patient populations. Atropine inhibited cont
ralateral secretion and lactoferrin production (p < 0.05) in patients
with symptomatic allergy. Conclusion: The induction of sneezing and of
atropine-inhibitable contralateral glandular secretion demonstrates t
hat allergic inflammation causes nasal hyperreactivity to bradykinin,
at least in part, by enhancing neuronal responsiveness.