Effects of Corticosteroid on Expression of IL-18 in the Airway Mucosa of Allergic Rhinitis Mouse Model.
- Author:
Si Whan KIM
1
;
Yoon Kyung JEON
;
Seok Chan HONG
;
Tae Bin WON
;
Yong Min KIM
;
Chae Seo RHEE
;
Yang Gi MIN
Author Information
1. Department of Otorhinolaryngology-Head and Neck Surgery, Seoul National University College of Medicine, Seoul, Korea. ygmin312@dreamwiz.com
- Publication Type:Original Article
- Keywords:
Allergic rhinitis;
Interleukin-18;
Glucocorticoid;
Corticosteroid
- MeSH:
Animals;
Asthma;
Bronchoalveolar Lavage Fluid;
Dexamethasone;
Eosinophils;
Inhalation;
Interleukin-18*;
Mice*;
Mucous Membrane*;
Nasal Lavage Fluid;
Ovalbumin;
Ovum;
Rhinitis*
- From:Journal of Rhinology
2006;13(2):101-106
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Background: This study aimed to investigate the release and response of IL-18 to steroid treatment in the allergic rhinitis (AR) mouse model. MATERIALS AND METHODS: BALB/c mice were sensitized systematically using an intraperitoneal ovalbumin (OVA) injection and locally by OVA inhalation. The steroid treatment group had an intraperitoneal dexamethasone injection. Symptom scores, eosinophil counts in nasal septal mucosa, and IL-18 concentrations in nasal and lung lavage fluid were analyzed. RESULTS: The symptom scores and eosinophil counts of the negative control and steroid treatment groups were significantly lower than those of the positive control group (p<.01). Meanwhile IL-18 concentrations of nasal lavage fluid of the three groups were not significantly different (56.68+/-9.57, 63.39+/-8.93, and 64.47+/-6.83 pg/mL, repectively). IL-18 concentration of lung lavage fluid was significantly different between the positive control and steroid treatment groups (430.75+/-154.54 and 69.94+/-14.26pg/mL respectively, p=.028). CONCLUSION: In this study, IL-18 concentration increased not in the nasal lavage fluid but in the lung lavage fluid in AR mouse model. The increased IL-18 concentration decreased after the steroid therapy. This result suggests that the role of IL-18 in the pathogenesis of AR may be different from that of asthma.
