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Effects of dexamethasone on the expression of transforming growth factor-beta in the mouse model of allergic rhinitis
Cited 11 time in
Web of Science
Cited 11 time in Scopus
- Authors
- Issue Date
- 2007
- Publisher
- Laryngoscope
- Citation
- Laryngoscope 2007;117:1323-1328
- Keywords
- Allergy ; dexamethasone ; TGF- ; CD4 T cell ; regulatory T cell ; Glucocorticoids/*therapeutic use ; Immunoglobulin E/metabolism ; Immunohistochemistry ; Leukocyte Count ; Mice, Inbred BALB C ; Nasal Mucosa/immunology/metabolism/pathology ; Ovalbumin/toxicity ; Reverse Transcriptase Polymerase Chain Reaction ; Transforming Growth Factor beta/*genetics/metabolism
- Abstract
- OBJECTIVES/HYPOTHESIS: This study aimed to evaluate the effect of dexamethasone on the expression of transforming growth factor (TGF)-beta in the mouse model of allergic rhinitis. STUDY DESIGN: Female BALB/c mice were randomly assigned to four groups, including two control groups and two treatment groups. METHODS: General sensitization and local challenge were performed with ovalbumin (OVA). In the treatment groups, dexamethasone was injected intraperitoneally 3 hours before general sensitization or local challenge. Symptom score, eosinophil infiltration, and immunostaining for TGF-beta1 and CD4 in nasal mucosa, and TGF-beta1 and OVA-specific immunoglobulin E (IgE) in sera were analyzed. RESULTS: Dexamethasone administration before general sensitization reduced the symptom score, OVA-specific IgE, and eosinophil infiltration and increased the serum level of TGF-beta1 significantly. Dexamethasone administration before local challenge reduced only the eosinophil infiltration significantly. Immunoreactivity of TGF-beta1 and CD4 was lower in both treatment groups. CONCLUSION: These results suggest that dexamethasone may play an important role in the regulation of allergic reactions by at least two mechanisms; one by suppressing allergic sensitization through decrease of CD4+ T cells and increase of TGF-beta, and the other by suppressing late allergic reactions through the inhibition of proliferation and chemotaxis of inflammatory cells such as eosinophils.
- ISSN
- 0023-852X (Print)
- Language
- English
- URI
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17762268
https://hdl.handle.net/10371/11174
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