title: Regulation of Trek1 expression in nasal mucosa with allergic rhinitis by specific immunotherapy.
abstract: Epithelial barrier dysfunction is involved in the pathogenesis of allergic disorders, such as nasal allergy. TWIK-related K(+) 1 (Trek1) potassium channels are required in the maintenance of the epithelial barrier function. This study aims to investigate the role of antigen-specific immunotherapy (SIT) in the regulation of Trek1 expression in the nasal mucosa. In this study, patients with nasal allergy were treated with SIT and/or Clostridium butyricum. The expression of Trek1 and histone demethylase 1 (HDAC1) in the nasal epithelia was assessed by real-time reverse transcription polymerase chain reaction and Western blotting. Serum cytokines were assessed by enzyme-linked immunosorbent assay. The results showed that Trek1 and HDAC1 were detected in the nasal epithelia. Trek1 was lower, whereas HDAC1 was higher in patients with allergic rhinitis as compared with healthy controls. Trek1-null RPMI2650 monolayers showed a markedly compromised epithelial barrier function. Treatment with SIT significantly increased the Trek1 levels in the nasal epithelia of allergic rhinitis patients that were further improved in conjunction of SIT and administration of probiotic C. butyricum. In conclusion, nasal epithelia express Trek1 that can be suppressed by allergic response. SIT can restore the expression of Trek1 in the nasal epithelia and can be further improved by conjunction with administration of C. butyricum.
authors.affiliation: Department of Otolaryngology, Liaocheng Second People's Hospital, Taishan Medical College, Liaocheng, China.
authors.forename: Yuzhi
authors.initials: Y
authors.lastname: Wang
authors.forename: Lingyan
authors.initials: L
authors.lastname: Lv
authors.forename: Hongrui
authors.initials: H
authors.lastname: Zang
authors.forename: Zhenfeng
authors.initials: Z
authors.lastname: Gao
authors.forename: Feng
authors.initials: F
authors.lastname: Zhang
authors.forename: Xingjie
authors.initials: X
authors.lastname: Wang
authors.forename: Xuanyan
authors.initials: X
authors.lastname: Zhou
mesh_terms: D000818:Animals; D019138:Antibodies, Blocking / Q000494:pharmacology; D002087:Butyrates / Q000494:pharmacology; D045744:Cell Line, Tumor; D003015:Clostridium Infections / Q000378:metabolism; D046972:Clostridium butyricum / Q000737:chemistry / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects*; D056284:Histone Deacetylase 1 / Q000378:metabolism; D056572:Histone Deacetylase Inhibitors / Q000494:pharmacology; D006801:Humans; D007167:Immunotherapy; D008297:Male; D008807:Mice, Inbred BALB C; D009297:Nasal Mucosa / Q000187:drug effects / Q000378:metabolism; D024683:Potassium Channels, Tandem Pore Domain / Q000235:genetics / Q000378:metabolism*; D065631:Rhinitis, Allergic / Q000188:drug therapy* / Q000378:metabolism; D018418:Th2 Cells / Q000378:metabolism
chemical_list: D019138:Antibodies, Blocking; D002087:Butyrates; D056572:Histone Deacetylase Inhibitors; D024683:Potassium Channels, Tandem Pore Domain; C103742:potassium channel protein TREK-1; C110550:HDAC1 protein, human; D056284:Histone Deacetylase 1
keywords: TWIK-related K(+) 1 potassium channels; allergy; epithelial barrier; immunotherapy; rhinitis