Reversal of Olfactory Disturbance in Allergic Rhinitis Related to OMP Suppression by Intranasal Budesonide Treatment
10.4168/aair.2020.12.1.110
- Author:
Ah Yeoun JUNG
1
;
Young Hyo KIM
Author Information
1. Department of Otorhinolaryngology, Inha University School of Medicine, Incheon, Korea. inhaorl@inha.ac.kr
- Publication Type:Original Article
- Keywords:
Olfactory mucosa;
olfaction disorders;
ovalbumin;
olfactory marker protein;
steroids;
allergic rhinitis;
quality of life;
odorants
- MeSH:
Animals;
Budesonide;
Hypersensitivity;
Inflammation;
Methimazole;
Mice;
Olfaction Disorders;
Olfactory Marker Protein;
Olfactory Mucosa;
Ovalbumin;
Ovum;
Quality of Life;
Rhinitis, Allergic;
Steroids
- From:Allergy, Asthma & Immunology Research
2020;12(1):110-124
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: We evaluated the severity of olfactory disturbance (OD) in the murine model of allergic rhinitis (AR) and local allergic rhinitis (LAR) in mice. We also investigated the therapeutic effect of an intranasal steroid on OD. METHODS: Forty BALB/c mice were divided into 5 groups (n = 8 for each). The control group was sensitized intraperitoneally (i.p.) and challenged intranasally (i.n.) with saline. Mice in the AR group got i.p. and i.n. ovalbumin (OVA) administration for AR induction. The LAR group was challenged i.n. with 1% OVA for inducing local nasal allergic inflammation, without inducing the systemic allergy. The OD group got an i.p. methimazole administration (75 mg/kg) to induce total destruction of olfactory mucosa. Mice in the intranasal budesonide group received i.n. budesonide (12.8 μg per time, 30 minutes after the i.n. OVA challenge) while using OVA to cause systemic allergies. We conducted a buried-food pellet test to functionally assess the degree of OD in each group by measuring the time taken until finding hidden food. We evaluated the damage to olfactory epithelium using histopathologic evaluation and compared the degree of olfactory marker protein (OMP) expression in olfactory epithelium using immunofluorescent staining. RESULTS: Mice of the AR (81.3 ± 19.8 seconds) and LAR groups (66.2 ± 12.7 seconds) spent significantly more time to detect the pellets than the control group (35.6 ± 12.2 seconds, P < 0.01). After treatment, the intranasal budesonide group exhibited significantly better results (35.8 ± 11.9 seconds) compared with the AR and LAR groups (P < 0.01). The AR and LAR groups showed considerable olfactory epithelial damage and suppression of OMP expression compared with the control group. In the intranasal budesonide group, the olfactory lesions and OMP expression had improved substantially. CONCLUSIONS: OD may be caused by olfactory epithelial damage and suppression of OMP expression in nasal allergic inflammation and could be reversed using an intranasal steroid.
