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| ファイル | 記述 | サイズ | フォーマット | |
|---|---|---|---|---|
| s41598-018-27408-y.pdf | 2.17 MB | Adobe PDF | 見る/開く |
| タイトル: | A bacterial metabolite ameliorates periodontal pathogen-induced gingival epithelial barrier disruption via GPR40 signaling |
| 著者: | Yamada, Miki Takahashi, Naoki Matsuda, Yumi Sato, Keisuke Yokoji, Mai Sulijaya, Benso Maekawa, Tomoki Ushiki, Tatsuo Mikami, Yoshikazu Hayatsu, Manabu Mizutani, Yusuke Kishino, Shigenobu    https://orcid.org/0000-0002-4587-2422 (unconfirmed)Ogawa, Jun https://orcid.org/0000-0003-2741-621X (unconfirmed)Arita, Makoto Tabeta, Koichi Maeda, Takeyasu Yamazaki, Kazuhisa |
| 著者名の別形: | 岸野, 重信 小川, 順 |
| 発行日: | 13-Jun-2018 |
| 出版者: | Springer Nature |
| 誌名: | Scientific Reports |
| 巻: | 8 |
| 論文番号: | 9008 |
| 抄録: | 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. |
| 著作権等: | © The Author(s) 2018. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
| URI: | http://hdl.handle.net/2433/235749 |
| DOI(出版社版): | 10.1038/s41598-018-27408-y |
| PubMed ID: | 29899364 |
| 出現コレクション: | 学術雑誌掲載論文等 |
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