Abstract
Objectives. Trichostatin A (TSA), an inhibitor of histone deacetylase, has been shown to play an important role in attenuating asthmatic inflammation. However, the effect of TSA in allergic rhinitis is not known. The aims of this study were to investigate the effect of TSA on allergic nasal inflammation and on the induction of regulatory T cells in a murine model of allergic rhinitis. Methods. BALB/c mice were sensitized intraperitoneally with ovalbumin (OVA) and then challenged intranasally with OVA. TSA (1 mg/kg) was given to the treatment group, and multiple parameters of allergic responses were evaluated to determine the effects of TSA on allergic rhinitis. Allergic nasal symptom scores, including frequency of rubbing and sneezing, were checked. Eosinophil infiltrations were stained with Chromotrope 2R, and the expression levels of OVA-specific IgE, T-helper 1 (Th1) cytokine (interferon-gamma [IFN-γ]), Th2 cytokines (interleukin [IL] 4 and IL-5) and Treg (Foxp3, IL-10, and transforming growth factor-beta [TGF-β]) were measured by quantitative reverse transcription-polymerase chain reaction or enzyme-linked immunosorbent assay. Results. TSA reduced the scores of allergic nasal symptoms and the amount of eosinophil infiltration into the nasal mucosa. TSA suppressed OVA-specific IgE levels and reduced expression of the IL-4 and IL-5. However, the expression of IFN-γ was unchanged in the treatment group. The levels of Foxp3, IL-10, and TGF-β were increased in pretreatment with TSA as compared to control group. Conclusion. This study shows that TSA induced antiallergic effects by decreasing eosinophilic infiltration and Th2 cytokines in a murine model of allergic rhinitis via regulation of Tregs. Thus, TSA may be considered a potentially therapeutic agent in treating allergic rhinitis.
| Original language | English |
|---|---|
| Pages (from-to) | 243-249 |
| Number of pages | 7 |
| Journal | Clinical and Experimental Otorhinolaryngology |
| Volume | 8 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 2015 Sep 1 |
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Keywords
- Allergic rhinitis
- Histone deacetylases
- Mice
- Ovalbumin
- Trichostatin A
ASJC Scopus subject areas
- Otorhinolaryngology
- Surgery
Cite this
Antiallergic effects of trichostatin A in a murine model of allergic rhinitis. / Cho, Jung Sun; Kang, Ju Hyung; Han, In Hye; Um, Ji Young; Park, Il Ho; Lee, Sang Hag; Lee, Heung Man.
In: Clinical and Experimental Otorhinolaryngology, Vol. 8, No. 3, 01.09.2015, p. 243-249.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Antiallergic effects of trichostatin A in a murine model of allergic rhinitis
AU - Cho, Jung Sun
AU - Kang, Ju Hyung
AU - Han, In Hye
AU - Um, Ji Young
AU - Park, Il Ho
AU - Lee, Sang Hag
AU - Lee, Heung Man
PY - 2015/9/1
Y1 - 2015/9/1
N2 - Objectives. Trichostatin A (TSA), an inhibitor of histone deacetylase, has been shown to play an important role in attenuating asthmatic inflammation. However, the effect of TSA in allergic rhinitis is not known. The aims of this study were to investigate the effect of TSA on allergic nasal inflammation and on the induction of regulatory T cells in a murine model of allergic rhinitis. Methods. BALB/c mice were sensitized intraperitoneally with ovalbumin (OVA) and then challenged intranasally with OVA. TSA (1 mg/kg) was given to the treatment group, and multiple parameters of allergic responses were evaluated to determine the effects of TSA on allergic rhinitis. Allergic nasal symptom scores, including frequency of rubbing and sneezing, were checked. Eosinophil infiltrations were stained with Chromotrope 2R, and the expression levels of OVA-specific IgE, T-helper 1 (Th1) cytokine (interferon-gamma [IFN-γ]), Th2 cytokines (interleukin [IL] 4 and IL-5) and Treg (Foxp3, IL-10, and transforming growth factor-beta [TGF-β]) were measured by quantitative reverse transcription-polymerase chain reaction or enzyme-linked immunosorbent assay. Results. TSA reduced the scores of allergic nasal symptoms and the amount of eosinophil infiltration into the nasal mucosa. TSA suppressed OVA-specific IgE levels and reduced expression of the IL-4 and IL-5. However, the expression of IFN-γ was unchanged in the treatment group. The levels of Foxp3, IL-10, and TGF-β were increased in pretreatment with TSA as compared to control group. Conclusion. This study shows that TSA induced antiallergic effects by decreasing eosinophilic infiltration and Th2 cytokines in a murine model of allergic rhinitis via regulation of Tregs. Thus, TSA may be considered a potentially therapeutic agent in treating allergic rhinitis.
AB - Objectives. Trichostatin A (TSA), an inhibitor of histone deacetylase, has been shown to play an important role in attenuating asthmatic inflammation. However, the effect of TSA in allergic rhinitis is not known. The aims of this study were to investigate the effect of TSA on allergic nasal inflammation and on the induction of regulatory T cells in a murine model of allergic rhinitis. Methods. BALB/c mice were sensitized intraperitoneally with ovalbumin (OVA) and then challenged intranasally with OVA. TSA (1 mg/kg) was given to the treatment group, and multiple parameters of allergic responses were evaluated to determine the effects of TSA on allergic rhinitis. Allergic nasal symptom scores, including frequency of rubbing and sneezing, were checked. Eosinophil infiltrations were stained with Chromotrope 2R, and the expression levels of OVA-specific IgE, T-helper 1 (Th1) cytokine (interferon-gamma [IFN-γ]), Th2 cytokines (interleukin [IL] 4 and IL-5) and Treg (Foxp3, IL-10, and transforming growth factor-beta [TGF-β]) were measured by quantitative reverse transcription-polymerase chain reaction or enzyme-linked immunosorbent assay. Results. TSA reduced the scores of allergic nasal symptoms and the amount of eosinophil infiltration into the nasal mucosa. TSA suppressed OVA-specific IgE levels and reduced expression of the IL-4 and IL-5. However, the expression of IFN-γ was unchanged in the treatment group. The levels of Foxp3, IL-10, and TGF-β were increased in pretreatment with TSA as compared to control group. Conclusion. This study shows that TSA induced antiallergic effects by decreasing eosinophilic infiltration and Th2 cytokines in a murine model of allergic rhinitis via regulation of Tregs. Thus, TSA may be considered a potentially therapeutic agent in treating allergic rhinitis.
KW - Allergic rhinitis
KW - Histone deacetylases
KW - Mice
KW - Ovalbumin
KW - Trichostatin A
UR - http://www.scopus.com/inward/record.url?scp=84940176087&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84940176087&partnerID=8YFLogxK
U2 - 10.3342/ceo.2015.8.3.243
DO - 10.3342/ceo.2015.8.3.243
M3 - Article
AN - SCOPUS:84940176087
VL - 8
SP - 243
EP - 249
JO - Clinical and Experimental Otorhinolaryngology
JF - Clinical and Experimental Otorhinolaryngology
SN - 1976-8710
IS - 3
ER -