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歯周炎の発症におけるヌクレオチド結合性多量体ドメイン1経路の役割
https://osaka-dent.repo.nii.ac.jp/records/2000108
https://osaka-dent.repo.nii.ac.jp/records/20001087da1a53a-29a6-4d5c-b1bd-b5c0bcf64ecd
| 名前 / ファイル | ライセンス | アクション |
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論文内容要旨・審査結果要旨 (276 KB)
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学位論文 (1.3 MB)
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| Item type | 学位論文 / Thesis or Dissertation(1) | |||||||||||
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| 公開日 | 2024-06-01 | |||||||||||
| 本文言語 | ||||||||||||
| 言語 | eng | |||||||||||
| タイトル | ||||||||||||
| タイトル | Role of the nucleotide-binding oligomerization domain-containing protein 1 pathway in the development of periodontitis | |||||||||||
| 言語 | en | |||||||||||
| タイトル | ||||||||||||
| タイトル | 歯周炎の発症におけるヌクレオチド結合性多量体ドメイン1経路の役割 | |||||||||||
| 言語 | ja | |||||||||||
| 著者 |
毛, 丹
× 毛, 丹
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| キーワード | ||||||||||||
| 言語 | en | |||||||||||
| 主題Scheme | Other | |||||||||||
| 主題 | Gingival epithelial cells | |||||||||||
| キーワード | ||||||||||||
| 言語 | en | |||||||||||
| 主題Scheme | Other | |||||||||||
| 主題 | Inflammation | |||||||||||
| キーワード | ||||||||||||
| 言語 | en | |||||||||||
| 主題Scheme | Other | |||||||||||
| 主題 | iE-DAP | |||||||||||
| キーワード | ||||||||||||
| 言語 | en | |||||||||||
| 主題Scheme | Other | |||||||||||
| 主題 | Innate immune response | |||||||||||
| 資源タイプ | ||||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_db06 | |||||||||||
| 資源タイプ | doctoral thesis | |||||||||||
| アクセス権 | ||||||||||||
| アクセス権 | open access | |||||||||||
| アクセス権URI | http://purl.org/coar/access_right/c_abf2 | |||||||||||
| 抄録 | ||||||||||||
| 内容記述タイプ | Abstract | |||||||||||
| 内容記述 | During innate immune defense, host pattern recognition receptors, including toll-like receptors and nucleotide-binding oligomerization domain-like receptors (NLRs), can activate downstream pathways by recognizing pathogen-associated molecular patterns produced by microorganisms, triggering immune responses. NOD1, an important cell membrane protein in the NLR-like receptor protein family, exerts anti-infective effects through γ-D-glutamyl-meso-diaminopimelic acid (iE-DAP) recognition. Oral epithelial cells resist bacterial invasion through iE-DAP-induced interleukin (IL)-8 production, recruiting neutrophils to sites of inflammation in response to bacterial threats to periodontal tissues. To date, the regulatory mechanisms of iE-DAP in gingival epithelial cells (GECs) are poorly understood. This study was conducted to investigate the role of the NOD1 pathway in the development of periodontitis by examining the effect of iE-DAP on IL-8 production in Ca9-22 cells.IL-8 production by iE-DAP-stimulated-Ca9-22 cells was assessed using an enzyme-linked immunosorbent assay. Phosphorylation levels of intracellular signaling molecules were evaluated using western blot analyses. iE-DAP induced NOD1 receptor expression in Ca9-22 cells. Additionally, iE-DAP induced expression of pro-IL-1β protein without extracellular secretion. Our results suggest that iE-DAP regulates IL-8 production by activating p38 mitogen-activated protein kinase (MAPK) and ERK1/2 signaling pathways. iE-DAP also promoted nuclear factor kappa-B p65 phosphorylation, facilitating its nuclear translocation. Notably, p38 MAPK and ERK1/2 inhibitors suppressed iE-DAP-stimulated IL-8 production, suggesting that JNK is not involved in this mechanism.Our results indicate that p38 MAPK and ERK1/2, but not JNK, are involved in innate immune responses in GECs. | |||||||||||
| 言語 | en | |||||||||||
| 学位名 | ||||||||||||
| 言語 | ja | |||||||||||
| 学位名 | 博士（歯学） | |||||||||||
| 学位授与機関 | ||||||||||||
| 学位授与機関識別子Scheme | kakenhi | |||||||||||
| 学位授与機関識別子 | 34408 | |||||||||||
| 言語 | ja | |||||||||||
| 学位授与機関名 | 大阪歯科大学 | |||||||||||
| 言語 | en | |||||||||||
| 学位授与機関名 | Osaka Dental University | |||||||||||
| 学位授与年月日 | ||||||||||||
| 学位授与年月日 | 2024-03-01 | |||||||||||
| 学位授与番号 | ||||||||||||
| 学位授与番号 | 甲第996号 | |||||||||||
| 権利 | ||||||||||||
| 言語 | en | |||||||||||
| 権利情報 | © 2024 Japanese Association for Oral Biology | |||||||||||
| 関連情報 | ||||||||||||
| 識別子タイプ | DOI | |||||||||||
| 関連識別子 | https://doi.org/10.1016/j.job.2023.12.008 | |||||||||||
| 関連情報 | ||||||||||||
| 関連名称 | Journal of Oral Biosciences. 2024, 66(1), p. 105-111. | |||||||||||
