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

doi:10.1080/09273948.2018.1560477

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 journal › Article › Academic › peer-review

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 language	English
Pages (from-to)	200-208
Number of pages	9
Journal	Ocular Immunology and Inflammation
Volume	28
Issue number	2
DOIs	https://doi.org/10.1080/09273948.2018.1560477
Publication status	Published - 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

Access to Document

10.1080/09273948.2018.1560477

Cite this

@article{a76e4a4666824836b059cf5f59432e0b,

title = "Decreased Expression of TGR5 in Vogt-Koyanagi-Harada (VKH) Disease",

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.",

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

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

note = "Funding Information: This work was support by National Natural Science Foundation Project (81470622); National Natural Science Foundation Project (81770913). Funding Information: This work was support by National Natural Science Foundation Project (81470622); National Natural Science Foundation Project (81770913). We want to thank all participants of the study. Publisher Copyright: {\textcopyright} 2018, {\textcopyright} 2018 Taylor & Francis Group, LLC.",

year = "2020",

month = feb,

day = "17",

doi = "10.1080/09273948.2018.1560477",

language = "English",

volume = "28",

pages = "200--208",

journal = "Ocular Immunology and Inflammation",

issn = "0927-3948",

publisher = "Routledge/Taylor & Francis Group",

number = "2",

}

TY - JOUR

T1 - Decreased Expression of TGR5 in Vogt-Koyanagi-Harada (VKH) Disease

AU - Yang, Jinglu

AU - Hu, Jianping

AU - Feng, Lujia

AU - Yi, Shenglan

AU - Ye, Zi

AU - Lin, Meng

AU - Liu, Xinglan

AU - Pu, Yanyu

AU - Kijlstra, Aize

AU - Yang, Peizeng

AU - Li, Hong

N1 - Funding Information: This work was support by National Natural Science Foundation Project (81470622); National Natural Science Foundation Project (81770913). Funding Information: This work was support by National Natural Science Foundation Project (81470622); National Natural Science Foundation Project (81770913). We want to thank all participants of the study. Publisher Copyright: © 2018, © 2018 Taylor & Francis Group, LLC.

PY - 2020/2/17

Y1 - 2020/2/17

N2 - 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.

AB - 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.

KW - TGR5

KW - VKH disease

KW - classically activated macrophages

KW - alternatively activated macrophages

KW - co-culture

KW - BILE-ACIDS

KW - INTESTINAL MACROPHAGES

KW - ACTIVATION

KW - RECEPTOR

KW - POLARIZATION

KW - INFLAMMATION

KW - PHENOTYPE

KW - INDUCE

KW - M1

U2 - 10.1080/09273948.2018.1560477

DO - 10.1080/09273948.2018.1560477

M3 - Article

C2 - 30794473

SN - 0927-3948

VL - 28

SP - 200

EP - 208

JO - Ocular Immunology and Inflammation

JF - Ocular Immunology and Inflammation

IS - 2

ER -