Effect of Route of Airway Allergen Challenge on Airway Inflammation and Hyperresponsiveness in Mouse Asthma Model.
- Author:
Dong Keun LEE
1
Author Information
1. Department of Pediatrics, Chung Ang University College of Medicine, Seoul, Korea. zf41643@netsgo.com
- Publication Type:Original Article
- Keywords:
Animal model;
Mouse;
Asthma;
Allergen challenges;
Airway;
Inflammation
- MeSH:
Animals;
Asthma*;
Bronchoalveolar Lavage Fluid;
Edema;
Eosinophils;
Inflammation*;
Lung;
Methacholine Chloride;
Mice*;
Models, Animal;
Mucus;
Ovalbumin;
Ovum;
Pneumonia
- From:Pediatric Allergy and Respiratory Disease
2003;13(4):263-270
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Airway hyperresponsiveness (AHR) and pulmonary inflammation with eosinophil infiltration and mucus hypersecretion are prominent features of asthma and can be reproduced in a murine model. There are some allergen challenge routes; intra-tracheal challenge and intra-nasal challenge are the main challenge routes. We examined whether these inflammatory responses varied by the routes of airway allergen challenges. METHODS: BALB/c mice after intraperitoneal (i.p.) ovalbumin (OVA) sensitization (day 0) were challenged with either intranasal (i.n.) or intratracheal (i.t.) OVA on day 8, day 15, day 18, and day 21. AHR to methacholine and lung inflammation were assessed 24 hours after the last OVA challenge on day 22. RESULTS: In bronchoalveolar lavage fluid, number of eosinophils were significantly greater in the intranasal OVA challenge group (4.8 +/- 0.9x10 (5) ) than in the intratracheal (2.0 +/- 0.3x10 (5) ) OVA challenge group (P< 0.01). Lung inflammatory cell infiltration and mucus hypersecretion were also greater in the intranasal OVA challenge group (P< 0.05). In contrast, AHR to methacholine (assessed by in vivo plethysmography) and peribronchial edema were significantly greater in the intratracheal OVA challenge group than intranasal OVA challenge group (P< 0.05). CONCLUSION: These data suggest the dissociation of eosinophilic airway inflammation from development of AHR and that peribronchial edema would contribute to the development of AHR.
