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Effects of dexamethasone on the expression of transforming growth factor-beta in the mouse model of allergic rhinitis

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Authors
Lee, Seung-Sin; Won, Tae-Bin; Kim, Jeong-Whun; Rhee, Chae-Seo; Lee, Chul-Hee; Hong, Seok-Chan; Min, Yang-Gi
Issue Date
2007
Publisher
Laryngoscope
Citation
Laryngoscope 2007;117:1323-1328
Keywords
AllergydexamethasoneTGF-CD4 T cellregulatory T cellGlucocorticoids/*therapeutic useImmunoglobulin E/metabolismImmunohistochemistryLeukocyte CountMice, Inbred BALB CNasal Mucosa/immunology/metabolism/pathologyOvalbumin/toxicityReverse Transcriptase Polymerase Chain ReactionTransforming 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

http://hdl.handle.net/10371/11174
DOI
https://doi.org/10.1097/MLG.0b013e318064e84d
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College of Medicine/School of Medicine (의과대학/대학원)Otorhinolaryngology (이비인후과학전공)Journal Papers (저널논문_이비인후과학전공)
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