Evidence map›Paper›PMID 29899364›Full record

ArticleScientific reports2018

A bacterial metabolite ameliorates periodontal pathogen-induced gingival epithelial barrier disruption via GPR40 signaling.

Miki Yamada, Naoki Takahashi, Yumi Matsuda, Keisuke Sato, Mai Yokoji, Benso Sulijaya, Tomoki Maekawa, Tatsuo Ushiki, Yoshikazu Mikami, Manabu Hayatsu and 7 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 66 citations in OpenAlex.

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  7. A Novel Postbiotic Reduces Canine Halitosis.Animals : an open access journal from MDPI · 2025
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  13. Frontiers in cellular and infection microbiology · 2024
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  17. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
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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

17 authors at 3 institutions in 1 country.

Miki YamadaResearch Unit for Oral-Systemic Connection, Division of Oral Science for Health Promotion, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Naoki TakahashiResearch Center for Advanced Oral Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan. takahashi-n@dent.niigata-u.ac.jp.
Yumi MatsudaResearch Unit for Oral-Systemic Connection, Division of Oral Science for Health Promotion, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Keisuke SatoResearch Unit for Oral-Systemic Connection, Division of Oral Science for Health Promotion, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Mai YokojiResearch Unit for Oral-Systemic Connection, Division of Oral Science for Health Promotion, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Benso SulijayaResearch Unit for Oral-Systemic Connection, Division of Oral Science for Health Promotion, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.ORCID 0000-0002-5976-430X
Tomoki MaekawaResearch Center for Advanced Oral Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Tatsuo UshikiDivision of Microscopic Anatomy and Bio-imaging, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Yoshikazu MikamiDivision of Microscopic Anatomy and Bio-imaging, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Manabu HayatsuDivision of Microscopic Anatomy and Bio-imaging, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Yusuke MizutaniDivision of Microscopic Anatomy and Bio-imaging, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Shigenobu KishinoDivision of Applied Life Sciences, Graduate School of Agriculture, Kyoto University, Kyoto, Japan.
Jun OgawaDivision of Applied Life Sciences, Graduate School of Agriculture, Kyoto University, Kyoto, Japan.
Makoto AritaLaboratory for Metabolomics, RIKEN Center for Integrative Medical Sciences, Kanagawa, Japan.
Koichi TabetaDivision of Periodontology, Department of Oral Biological Science, Niigata University Faculty of Dentistry, Niigata, Japan.
Takeyasu MaedaResearch Center for Advanced Oral Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Kazuhisa YamazakiResearch Unit for Oral-Systemic Connection, Division of Oral Science for Health Promotion, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan. kaz@dent.niigata-u.ac.jp.
Niigata University · JPKyoto University · JPRIKEN Center for Integrative Medical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several studies have demonstrated the remarkable properties of microbiota and their metabolites in the pathogenesis of several inflammatory diseases. 10-Hydroxy-cis-12-octadecenoic acid (HYA), a bioactive metabolite generated by probiotic microorganisms during the process of fatty acid metabolism, has been studied for its protective effects against epithelial barrier impairment in the intestines. Herein, we examined the effect of HYA on gingival epithelial barrier function and its possible application for the prevention and treatment of periodontal disease. We found that GPR40, a fatty acid receptor, was expressed on gingival epithelial cells; activation of GPR40 by HYA significantly inhibited barrier impairment induced by Porphyromonas gingivalis, a representative periodontopathic bacterium. The degradation of E-cadherin and beta-catenin, basic components of the epithelial barrier, was prevented in a GPR40-dependent manner in vitro. Oral inoculation of HYA in a mouse experimental periodontitis model suppressed the bacteria-induced degradation of E-cadherin and subsequent inflammatory cytokine production in the gingival tissue. Collectively, these results suggest that HYA exerts a protective function, through GPR40 signaling, against periodontopathic bacteria-induced gingival epithelial barrier impairment and contributes to the suppression of inflammatory responses in periodontal diseases.

Indexed as

AnimalsBacteriaCaco-2 CellsCadherinsCell LineCytokinesEpithelial CellsGene ExpressionGingivaHumansMaleMice, Inbred C57BLOleic AcidsPeriodontal DiseasesPeriodontitisPorphyromonas gingivalis10-hydroxy-12-octadecenoic acidCadherinsCytokinesFFAR1 protein, humanOleic AcidsReceptors, G-Protein-Coupled

Identifiers

PMID29899364
PMCPMC5998053
OpenAlexW2805667791

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.