In:
The Clinical Respiratory Journal, Wiley, Vol. 10, No. 3 ( 2016-05), p. 371-379
Abstract:
The aim of this study is to investigate the expression pattern of histone deacetylase 9 in peripheral blood of patients with allergic asthma and its regulatory effect on the balance of Th 17/Treg cells involved in the pathogenesis of asthma. Methods flap‐Ub promoter‐GFP‐WRE vector was used to construct the J urkat‐ HA ‐ FOXP 3 cell line. After histone deacetylase inhibitor‐trichostatin A ( TSA ) treatment, FOXP 3 and ROR γt expression were detected by real‐time‐polymerase chain reaction ( RT ‐ PCR ). BALB /c mice were randomly assigned to control group, TSA treatment and the asthma group. Serum Immunoglobulin E (IgE) was detected with enzyme‐linked immunosorbent assay ( ELISA ), airway inflammation in lung tissue evaluated by haematoxylin/eosin staining, bronchoalveolar lavage fluid ( BALF ) cell number and differential counted, interleukin ( IL )‐17 A and TGF ‐β concentrations in BALF measured with ELISA , and expression of ROR γt and FOXP 3 messenger RNA ( mRNA )measured by RT ‐ PCR . Forty‐seven patients with asthma were recruited and assigned to intermittent, mild and moderate–severe group. GATA 3, IL ‐4, histone deacetylases ( HDAC ) 9 mRNA expression level were measured by RT ‐ PCR . Results After TSA treatment, FOXP 3 mRNA level was upregulated, while ROR γt mRNA level was downregulated. FOXP 3 protein level was also upregulated by TSA . In vivo , TSA treatment can inhibit IL ‐17 but promote transforming growth factor‐beta production in the BALF of asthma mice, and inhibited the expression of Th 17 cells and ROR γt mRNA in lung; also can promote Foxp 3 mRNA expression. GATA 3, IL ‐4 mRNA expression levels were upregulated in patients with asthma than the healthy control. HDAC 9 mRNA expression level was associated with the severity of disease. Conclusion The histone deacetylase inhibitor TSA can regulate the balance of Th 17/Treg in asthma by regulating the activity of histone deacetylase.
Type of Medium:
Online Resource
ISSN:
1752-6981
,
1752-699X
DOI:
10.1111/crj.2016.10.issue-3
Language:
English
Publisher:
Wiley
Publication Date:
2016
detail.hit.zdb_id:
2442214-9
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