title: Transforming growth factor-β1 promotes Treg commitment in nasal polyposis after intranasal steroid treatment.
abstract: BACKGROUND
  A predominant Th17 population and impaired Treg function is the marker of nasal polyposis (NP) in Chinese patients. TGF-β1, a multifunction cytokine, is a vital factor involved in inducing or restricting specific Th cell development. However, its role in NP has still not been well understood.
  
  
  METHODS
  In a double-blind trial, 30 subjects were randomized into 2 groups (15 steroid-treated NP, 15 untreated NP), and 15 normal subjects were allocated as control group. We analyzed the expression of TGF-β1, p-Smad2, p-STAT3, Smad7, SOCS3, IL-10, IL-17A, Foxp3, and RORc in the NP tissue of Chinese patients using mRNA and protein detection methods.
  
  
  RESULTS
  TGF-β1, p-Smad2, IL-10, SOCS3, and Foxp3 expression was higher in steroid-treated NP patients than in untreated NP patients. Conversely, expression of p-STAT3, Smad7, IL-17A, and RORc was higher in untreated NP patients than in steroid-treated NP patients, demonstrating that TGF-β1 was more likely to contribute to Treg commitment in Chinese NP patients after intranasal steroid treatment.
  
  
  CONCLUSIONS
  TGF-β1 may be a signature Treg cytokine, which is valuable for obtaining a clear understanding of the pathogenesis of NP. Moreover, intranasal steroid treatment attenuated the chronic inflammatory response in these patients by promoting Smad-dependent Treg functions and reducing STAT3-mediated Th17 reactions.
authors.affiliation: Department of Otorhinolaryngology-Head and Neck Surgery, The First Affiliated Hospital of Chongqing Medical University, 1# Youyi Road, Yuzhong District, Chongqing 400016, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Kou
authors.forename: Guo-Hua
authors.initials: GH
authors.lastname: Hu
authors.forename: Hong-Bing
authors.initials: HB
authors.lastname: Yao
authors.forename: Xiao-Qiang
authors.initials: XQ
authors.lastname: Wang
authors.forename: Yang
authors.initials: Y
authors.lastname: Shen
authors.forename: Hou-Yong
authors.initials: HY
authors.lastname: Kang
authors.forename: Su-Ling
authors.initials: SL
authors.lastname: Hong
mesh_terms: D000281:Administration, Intranasal; D000328:Adult; D002681:China; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D016753:Interleukin-10 / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009298:Nasal Polyps / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology*; D050796:STAT3 Transcription Factor / Q000378:metabolism; D051899:Smad2 Protein / Q000378:metabolism; D051906:Smad7 Protein / Q000378:metabolism; D013256:Steroids / Q000008:administration & dosage / Q000627:therapeutic use*; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000473:pathology* / Q000502:physiology*; D058504:Th17 Cells / Q000473:pathology / Q000502:physiology
chemical_list: D020381:Interleukin-17; C497782:SMAD2 protein, human; C497806:SMAD7 protein, human; C106644:SOCS3 protein, human; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D051899:Smad2 Protein; D051906:Smad7 Protein; D013256:Steroids; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D016753:Interleukin-10