Decreased Expression of TGR5 in Vogt-Koyanagi-Harada (VKH) Disease

Jinglu Yang, Jianping Hu, Lujia Feng, Shenglan Yi, Zi Ye, Meng Lin, Xinglan Liu, Yanyu Pu, Aize Kijlstra, Peizeng Yang, Hong Li*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

4 Citations (Web of Science)

Abstract

Purpose: To investigate the role of G-protein-coupled bile acid receptor-1, Gpbar1 (TGR5) in the pathogenesis of Vogt-Koyanagi-Harada (VKH) disease. Methods: The mRNA level of TGR5, iNOS, Arg1, CD16, and CD206 in macrophages was assayed by real-time PCR. ELISA was used to detect the production of cytokines in cell culture supernatants. The frequencies of CD4(+)IFN-gamma(+) and CD4(+) IL-17(+) T cells were tested by flow cytometry. Results: A decreased expression of TGR5 in M1 macrophages was observed in active VKH patients as compared with normal controls. TGR5 stimulation of M1 macrophages with INT-777 caused a shift of the inflammatory M1 toward the anti-inflammatory M2 macrophage subtype. TGR5 activation of macrophages co-cultured with CD4(+) T cells inhibited Th1 and Th17 polarization, as well as the release of IFN-gamma and IL-17 in the culture supernatant. Conclusion: Our results show that a decreased TGR5 expression might contribute to the pathogenesis of VKH disease.

Original languageEnglish
Pages (from-to)200-208
Number of pages9
JournalOcular Immunology and Inflammation
Volume28
Issue number2
DOIs
Publication statusPublished - 17 Feb 2020

Keywords

  • TGR5
  • VKH disease
  • classically activated macrophages
  • alternatively activated macrophages
  • co-culture
  • BILE-ACIDS
  • INTESTINAL MACROPHAGES
  • ACTIVATION
  • RECEPTOR
  • POLARIZATION
  • INFLAMMATION
  • PHENOTYPE
  • INDUCE
  • M1

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