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In allergen challenged animal models, eosinophils localize to airway nerves leading to vagally-mediated hyperreactivity. We hypothesized that in allergic rhinitis eosinophils recruited to nasal nerves resulted in neural hyperreactivity. Patients with persistent allergic rhinitis (n=12), seasonal allergic rhinitis (n=7) and controls (n=10) were studied. Inferior nasal turbinate biopsies were obtained before, 8 and 48h after allergen challenge. Eight hours after allergen challenge eosinophils localized to nerves in both rhinitis groups; this was sustained through 48h. Bradykinin challenge, with secretion collection on the contralateral side, was performed to demonstrate nasal nerve reflexes. Twenty fourhours after allergen challenge, bradykinin induced a significant increase in secretions, indicating nasal hyperreactivity. Histological studies showed that nasal nerves expressed both vascular cell adhesion molecule-1 (VCAM-1) and chemokine (C-C motif) ligand 26 (CCL-26). Hence, after allergen challenge eosinophils are recruited and retained at nerves and so may be a mechanism for neural hyperreactivity., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Introduction: Neurally mediated secretory hyperresponsiveness is a feature of allergic rhinitis (AR). Muscarinic M2 receptors are inhibitory autoreceptors which limit acetylcholine release at postganglionic parasympathetic nerve terminals, dysfunction of which has been implicated as a cause of bronchial hyperresponsiveness in asthma. The purpose of this study was to investigate the presence and function of M2 receptors in the human nose., Methods: In the first part of the study, nasal biopsies from subjects with AR (n = 12) and normal controls (n = 10) were examined for the presence of M2 receptor mRNA using polymerase chain reaction (PCR). In the second part, subjects with symptomatic AR (n = 17), with established contralateral secretory reflexes to bradykinin, underwent unilateral bradykinin challenge after premedication with pilocarpine, a M2 receptor agonist. The effect of pilocarpine on contralateral secretory reflexes was studied., Results: M2 receptor mRNA was detected in 12 subjects (54%). Pilocarpine premedication led to a significant reduction of the contralateral secretory reflex to bradykinin., Conclusion: M2 receptors are present in the human nasal mucosa, though not universally. The function of M2 receptors in subjects with AR can be demonstrated using pilocarpine, however, more work is required to define their importance and potential role in nasal hyperresponsiveness

Background: Nasal secretory hyperresponsiveness is well documented in allergic rhinitis, and is mediated in part by neural mechanisms. In contrast, reflex-mediated congestion is poorly documented in both normal and allergic subjects., Objective: To characterize congestive responses to unilateral nasal bradykinin challenge in normal and allergic subjects, and to investigate whether congestive hyperresponsiveness is present in allergic rhinitis., Methods: Normal subjects (n = 13), and subjects with out-of-season seasonal allergic rhinitis (SAR) (n = 16) underwent a unilateral nasal challenge protocol using filter paper disks, using Hartman's solution and bradykinin as challenge substances. Congestive responses were measured using acoustic rhinometry., Results: Normal subjects demonstrated a transient ipsilateral congestive response, and a circumscribed contralateral congestive response away from the major flow limiting section. Subjects with SAR demonstrated a more persistent ipsilateral congestive response, and a more pronounced, generalized contralateral congestive response affecting all areas of the contralateral nasal cavity. Significant differences were present between normal and SAR subjects., Conclusion: Congestive reflexes are present in normal and allergic subjects. Congestive hyperresponsiveness is present in allergic rhinitis.