Author/Authors :
Thornton، نويسنده , , Margaret A. and Akasheh، نويسنده , , Nadim and Walsh، نويسنده , , Marie-Therese and Moloney، نويسنده , , Michael and Sheahan، نويسنده , , Patrick O. and Smyth، نويسنده , , Claire M. and Walsh، نويسنده , , Rory McConn and Morgan، نويسنده , , Ross M. and Curran، نويسنده , , David R. and Walsh، نويسنده , , Michael T. and Gleich، نويسنده , , Gerald J. and Costello، نويسنده , , R، نويسنده ,
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 48 h after allergen challenge. Eight hours after allergen challenge eosinophils localized to nerves in both rhinitis groups; this was sustained through 48 h. Bradykinin challenge, with secretion collection on the contralateral side, was performed to demonstrate nasal nerve reflexes. Twenty four hours 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.
