Transforming growth factor-β1 promotes Treg commitment in nasal polyposis after intranasal steroid treatment

Inflamm Res. 2013 Mar;62(3):283-9. doi: 10.1007/s00011-012-0576-x. Epub 2012 Nov 22.

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.

Publication types

  • Randomized Controlled Trial

MeSH terms

  • Administration, Intranasal
  • Adult
  • China
  • Double-Blind Method
  • Female
  • Humans
  • Interleukin-10 / metabolism
  • Interleukin-17 / metabolism
  • Male
  • Middle Aged
  • Nasal Polyps / drug therapy*
  • Nasal Polyps / metabolism
  • Nasal Polyps / physiopathology*
  • STAT3 Transcription Factor / metabolism
  • Smad2 Protein / metabolism
  • Smad7 Protein / metabolism
  • Steroids / administration & dosage
  • Steroids / therapeutic use*
  • Suppressor of Cytokine Signaling 3 Protein
  • Suppressor of Cytokine Signaling Proteins / metabolism
  • T-Lymphocytes, Regulatory / pathology*
  • T-Lymphocytes, Regulatory / physiology*
  • Th17 Cells / pathology
  • Th17 Cells / physiology

Substances

  • Interleukin-17
  • SMAD2 protein, human
  • SMAD7 protein, human
  • SOCS3 protein, human
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Smad2 Protein
  • Smad7 Protein
  • Steroids
  • Suppressor of Cytokine Signaling 3 Protein
  • Suppressor of Cytokine Signaling Proteins
  • Interleukin-10