The G-protein-coupled bile acid receptor Gpbar1 (TGR5) inhibits gastric inflammation through antagonizing NF-κB signaling pathway
Open accessAbstract
Gpbar1 (TGR5), a membrane-bound bile acid receptor, is well-known for its roles in regulation of energy homeostasis and glucose metabolism. Here, we show that mice lacking TGR5 were much more susceptible to lipopolysaccharide (LPS)-induced acute gastric inflammation than wild-type (WT) mice and TGR5 is a negative regulator of gastric inflammation through antagonizing NF-κB signaling pathway. We found that the treatment of TGR5 ligands 23(S)-mCDCA and GPBARA (3-(2-Chlorophenyl)-N-(4-chlorophenyl)-N,5-dimethylisoxazole-4-carboxamide) suppressed gene and protein expression mediated by NF-κB signaling. TGR5 overexpression with ligand treatment inhibited gene expression of interferon-inducible protein 10 (IP-10), TNF-α, and chemoattractant protein-1 (MCP-1) induced by LPS. Furthermore, we revealed that TGR5 activation antagonized NF-κB signaling pathway through suppressing its transcription activity, the phosphorylation of IκBα and p65 translocation, which suggests that TGR5 antagonizes gastric inflammation at least in part by inhibiting NF-κB signaling. These findings identify TGR5 as a negative mediator of gastric inflammation that may serve as an attractive therapeutic tool for human gastric inflammation and cancer.
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Activation of GPBAR1 on macrophages and Kupffer cells by synthetic agonists inhibits LPS-induced pro-inflammatory cytokines by interfering with NF-κB-dependent transcription.
“activation of GPBAR1 on macrophages and Kupffer cells by synthetic agonists inhibits the expression of LPS-induced pro-inflammatory cytokines by interfering with NF-κB-dependent transcription.”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as C. Guo et al., 2015
This inhibition has been linked to direct inhibition of NF-κB activation but is also consistent with transcriptional competition between NF-κB and CREB.
“This has been linked to direct inhibition of NF-κB activation, but is also consistent with a model of transcriptional competition between NF-κB and the cAMP-activated transcription factor cAMP response element binding protein (CREB) (C. Guo et al., 2015; Kawamata et al., 2003; Keitel et al., 2008; Pols et al., 2011; Y.-D. Wang et al., 2011; Wen et al., 2010).”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as C. Guo et al., 2015
Gpbar1−/− mice develop more severe disease than wildtype controls in several animal models of inflammatory disorder, including colitis, hepatitis, and gastritis.
“Gpbar1−/− mice, like their Nr1h4−/− counterparts, develop more severe disease than wildtype controls in several animal models of inflammatory disorder, including colitis, hepatitis and gastritis (Cipriani et al., 2011; C. Guo et al., 2015; Y.-D. Wang et al., 2011).”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as C. Guo et al., 2015
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- Authors
- Guo, C., Qi, H., Yu, Y., Zhang, Q., Su, J., Yu, D., Huang, W., Chen, W.-D., & Wang, Y.-D.
- Affiliations
- State Key Laboratory of Chemical Resource Engineering (CN)
- Henan University (CN)
- State University of New York (US)
- City Of Hope National Medical Center (US)
- Corresponding author
- Wang, Yan-Dong
- Venue
- Frontiers in Pharmacology
- Publisher
- Frontiers Media SA
- Published
- 2015-12-11
- Volume
- 6
- Pages
- 287-287
- ISSN
- 1663-9812 (ISSN-L)
- PMC
- PMC4675858
- OpenAlex
- W2191241037
- Cited by
- 95
- References
- 34
- Citations by year
- 2026: 6 · 2025: 3 · 2024: 7 · 2023: 6 · 2022: 15 · 2021: 9 · 2020: 17 · 2019: 9 · 2018: 11 · 2017: 8 · 2016: 4
- FWCI
- 3.35
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Pharmacology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (81370537, 81270522, 81472232)
- Topics
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- TGR5, bile acid receptors, gastritis, NF-κB signaling, lipopolysaccharide, IκBα phosphorylation, CXCL10, TNF-α, MCP-1, anti-inflammatory therapy
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