Evidence map›Paper›PMID 23566200›Full record

Trial reportImmunology2013

TGR5 signalling inhibits the production of pro-inflammatory cytokines by in vitro differentiated inflammatory and intestinal macrophages in Crohn's disease.

Kazuaki Yoneno, Tadakazu Hisamatsu, Katsuyoshi Shimamura, Nobuhiko Kamada, Riko Ichikawa, Mina T Kitazume, Maiko Mori, Michihide Uo, Yuka Namikawa, Katsuyoshi Matsuoka and 5 more

Open access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in Immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
135citing papers in PubMed, 2 pooled it
5.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

135 citing papers in PubMed, 2 syntheses or guidelines pooled it, 206 citations in OpenAlex.

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  10. Short-chain Fatty Acids and Bile Acids Signaling in Chronic Hepatitis B.Journal of clinical and translational hepatology · 2026
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75 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 2 countries.

Kazuaki YonenoDivision of Gastroenterology and Hepatology, Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Tadakazu Hisamatsu
Katsuyoshi Shimamura
Nobuhiko Kamada
Riko Ichikawa
Mina T Kitazume
Maiko Mori
Michihide Uo
Yuka Namikawa
Katsuyoshi Matsuoka
Toshiro Sato
Kazutaka Koganei
Akira Sugita
Takanori Kanai
Toshifumi Hibi
Keio University · JPYokohama Municipal Citizen's Hospital · JPUniversity of Michigan–Ann Arbor · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bile acids (BAs) play important roles not only in lipid metabolism, but also in signal transduction. TGR5, a transmembrane receptor of BAs, is an immunomodulative factor, but its detailed mechanism remains unclear. Here, we aimed to delineate how BAs operate in immunological responses via the TGR5 pathway in human mononuclear cell lineages. We examined TGR5 expression in human peripheral blood monocytes, several types of in vitro differentiated macrophages (Mϕs) and dendritic cells. Mϕs differentiated with macrophage colony-stimulating factor and interferon-γ (Mγ-Mϕs), which are similar to the human intestinal lamina propria CD14(+) Mϕs that contribute to Crohn's disease (CD) pathogenesis by production of pro-inflammatory cytokines, highly expressed TGR5 compared with any other type of differentiated Mϕ and dendritic cells. We also showed that a TGR5 agonist and two types of BAs, deoxycholic acid and lithocholic acid, could inhibit tumour necrosis factor-α production in Mγ-Mϕs stimulated by commensal bacterial antigen or lipopolysaccharide. This inhibitory effect was mediated by the TGR5-cAMP pathway to induce phosphorylation of c-Fos that regulated nuclear factor-κB p65 activation. Next, we analysed TGR5 levels in lamina propria mononuclear cells (LPMCs) obtained from the intestinal mucosa of patients with CD. Compared with non-inflammatory bowel disease, inflamed CD LPMCs contained more TGR5 transcripts. Among LPMCs, isolated CD14(+) intestinal Mϕs from patients with CD expressed TGR5. In isolated intestinal CD14(+) Mϕs, a TGR5 agonist could inhibit tumour necrosis factor-α production. These results indicate that TGR5 signalling may have the potential to modulate immune responses in inflammatory bowel disease.

Indexed as

Antigens, BacterialCells, CulturedCholagogues and CholereticsCrohn DiseaseCytokinesDendritic CellsDeoxycholic AcidDetergentsFemaleGene Expression RegulationHumansInterferon-gammaIntestinal MucosaLipopolysaccharidesLithocholic AcidMacrophage Colony-Stimulating FactorAntigens, BacterialCholagogues and CholereticsCytokinesDeoxycholic AcidDetergentsGPBAR1 protein, humanIFNG protein, humanInterferon-gammaLipopolysaccharidesLithocholic AcidMacrophage Colony-Stimulating FactorProto-Oncogene Proteins c-fosReceptors, G-Protein-CoupledRELA protein, humanTranscription Factor RelA

Identifiers

PMID23566200
PMCPMC3634536
OpenAlexW1967283548

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.