| Literature DB >> 23518598 |
Margaret A Thornton1, Nadim Akasheh2, Marie-Therese Walsh3, Michael Moloney3, Patrick O Sheahan1, Claire M Smyth3, Rory McConn Walsh1, Ross M Morgan3, David R Curran3, Michael T Walsh1, Gerald J Gleich4, Richard W Costello3.
Abstract
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.Entities:
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Year: 2013 PMID: 23518598 DOI: 10.1016/j.clim.2013.02.008
Source DB: PubMed Journal: Clin Immunol ISSN: 1521-6616 Impact factor: 3.969