Effect of dexamethasone on the expression of Tregs in allergic rhinitis mice.
- Author:
Tingting JIANG
;
Weihua WANG
;
Zhenghua ZHU
;
Liwei ZHU
;
Zhaoxin MA
- Publication Type:Journal Article
- MeSH:
Administration, Intranasal;
Animals;
Dexamethasone;
pharmacology;
Disease Models, Animal;
Flow Cytometry;
Forkhead Transcription Factors;
metabolism;
Inflammation;
drug therapy;
Mice;
Mice, Inbred BALB C;
Nasal Mucosa;
drug effects;
Ovalbumin;
RNA, Messenger;
Rhinitis, Allergic;
drug therapy;
T-Lymphocytes, Regulatory;
drug effects
- From:
Journal of Clinical Otorhinolaryngology Head and Neck Surgery
2015;29(12):1121-1125
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of dxamethasone (DEX) on the expression of Tregs in allergic rhinitis (AR) mice, and explore the mechanism of glucocorticoid in the treatment of AR.
METHOD:AR murine model was established by sensitization and challenge with OVA, besides intervention treatment with DEX was carried out in AR model. The behavior observation was used to evaluate the improvement effect of DEX on AR symptoms. The morphological characteristics of nasal tissues were observed by HE staining after fixation and decalcification. The mononuclear cells were obtained by grinding spleens, and the total RNA was extracted for reverse transcriptase polymerase chain reaction to investigate the level of mRNA expression of Foxp3. The changes of CD4+ Foxp3+ Tcells in spleen of mice were analyzed by flow cytometry.
RESULT:BALB/c mice received OVA sensitization followed by OVA intranasal challenge, the frequencies of sneezing and nose-scratching increased significantly in AR group (44. 50 ± 5. 61 and 72. 94 ± 8. 76) compared with control group (12. 68 ± 1. 87 and 26. 76 ± .2. 89), P<0. 01; The frequencies decreased significantly in DEX group (26. 04 ± 3. 93 and 56. 79 ± 5. 64), P< 0. 05 compared with AR group. The continuity of nasal mucosa ciliated columnar epithelium in AR group was destroyed and appeared to be repaired in DEX group. Inflammatory cells infiltration was also markedly decreased by DEX treatment. The proportion of CD4+ Foxp3+ T cells in AR group (3. 89 ± 0. 39)% decreased, P<0. 01 vs control group (4. 63 ± 0. 15) %. DEX treatment induced production of Tregs (6. 89 ± 0. 49)%, P<0. 05 vs control group. DEX significantly increased the expression of Foxp3 mRNA (P<0. 05) compared with AR and control group.
CONCLUSION:DEX reduce upper airway allergic inflammation effectively, which may be mediated by promoting the expression of Foxp3 and inducing the amplification of Tregs in vivo.
