Antiallergic effects of trichostatin A in a murine model of allergic rhinitis

Jung Sun Cho, Ju Hyung Kang, In Hye Han, Ji Young Um, Il Ho Park, Sang Hag Lee, Heung Man Lee

Research output: Contribution to journalArticle

2 Citations (Scopus)

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 languageEnglish
Pages (from-to)243-249
Number of pages7
JournalClinical and Experimental Otorhinolaryngology
Volume8
Issue number3
DOIs
Publication statusPublished - 2015 Sep 1

Fingerprint

trichostatin A
Anti-Allergic Agents
Ovalbumin
Nose
Interleukin-5
Cytokines
Eosinophils
Interleukin-4
Transforming Growth Factor beta
Interleukin-10
Immunoglobulin E
Interferon-gamma
Allergic Rhinitis
Inflammation
Sneezing
Histone Deacetylase Inhibitors
Nasal Mucosa
Regulatory T-Lymphocytes
Reverse Transcription

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 journalArticle

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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.",
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AU - Han, In Hye

AU - Um, Ji Young

AU - Park, Il Ho

AU - Lee, Sang Hag

AU - Lee, Heung Man

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KW - Ovalbumin

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