○種別 (必須): | □ | 学術論文 (審査論文)
| [継承] |
○言語 (必須): | □ | 英語
| [継承] |
○招待 (推奨): |
○審査 (推奨): |
○カテゴリ (推奨): |
○共著種別 (推奨): |
○学究種別 (推奨): |
○組織 (推奨): |
○著者 (必須): | 1. | (英) Suryono (日) (読)
○役割 (任意): |
○貢献度 (任意): |
○学籍番号 (推奨): |
| [継承] |
| 2. | 木戸 淳一
○役割 (任意): |
○貢献度 (任意): |
○学籍番号 (推奨): |
| [継承] |
| 3. | (英) Hayashi Noriko (日) (読)
○役割 (任意): |
○貢献度 (任意): |
○学籍番号 (推奨): |
| [継承] |
| 4. | 片岡 正俊
○役割 (任意): |
○貢献度 (任意): |
○学籍番号 (推奨): |
| [継承] |
| 5. | 永田 俊彦
○役割 (任意): |
○貢献度 (任意): |
○学籍番号 (推奨): |
| [継承] |
○題名 (必須): | □ | (英) Effect of Porphyromonas gingivalis lipopolysaccharide, tumor necrosis factor-alpha, and interleukin-1beta on calprotectin release in human monocytes (日)
| [継承] |
○副題 (任意): |
○要約 (任意): | □ | (英) Calprotectin is a major cytosolic protein of monocytes, granulocytes, and epithelial cells. It is known that calprotectin is released in inflammatory tissues and detected in gingival crevicular fluid (GCF) of periodontitis patients at high levels. The origin of calprotectin in GCF and its regulation in periodontal disease are unknown. In this study, we investigated the distribution of calprotectin in gingival tissue with inflammation and the induction of calprotectin release from human monocytes by lipopolysaccharide of Porphyromonas gingivalis (P-LPS), tumor necrosis factor-alpha (TNF-alpha), or interleukin-1beta (IL-1beta). Gingival tissues were obtained from a healthy donor and a periodontitis patient and calprotectin in gingival tissues was examined by immunohistochemical staining. Monocytes were isolated from the peripheral blood of healthy donors and cultured with P-LPS, TNF-alpha or IL-1beta for 30 minutes to 4 hours. The content of calprotectin in the cell and medium fractions was determined by enzyme-linked immunosorbent assay (ELISA). Calprotectin was markedly detected at the epithelial and adjacent connective tissue with many inflammatory cells in the gingival tissue from the periodontitis patient. P-LPS increased calprotectin release from monocytes to the maximum level after 30 minutes of treatment and its level was elevated to about 2- to 3-fold of the control level in a dose-dependent manner (1 to 1,000 ng/ml). When the effect of TNF-alpha and IL-1beta on calprotectin release was investigated, calprotectin release significantly increased to about 2.2- and 1.5-fold that of the control level, respectively. These results demonstrate that calprotectin release from monocytes is induced by P-LPS, TNF-alpha, and IL-1beta, which in turn, cause and aggravate periodontal disease. (日)
| [継承] |
○キーワード (推奨): | 1. | (英) calprotectin (日) (読)
| [継承] |
| 2. | (英) gingival crevicular fluid/analysis (日) (読)
| [継承] |
| 3. | (英) interleukin-1 (日) (読)
| [継承] |
| 4. | (英) monocytes physiopathology (日) (読)
| [継承] |
| 5. | (英) periodontitis/physiopatholoogy (日) (読)
| [継承] |
| 6. | (英) Porphyromonas gingivalis (日) (読)
| [継承] |
| 7. | (英) tumor necrosis factor (日) (読)
| [継承] |
○発行所 (推奨): |
○誌名 (必須): | □ | Journal of Periodontology (American Academy of Periodontology)
(pISSN: 0022-3492, eISSN: 1943-3670)
○ISSN (任意): | □ | 0022-3492
ISSN: 0022-3492
(pISSN: 0022-3492, eISSN: 1943-3670) Title: Journal of periodontologyTitle(ISO): J PeriodontolSupplier: American Academy of PeriodontologyPublisher: Wiley (NLM Catalog)
(Wiley)
(Scopus)
(CrossRef)
(CrossRef)
(Scopus information is found. [need login])
| [継承] |
| [継承] |
○巻 (必須): | □ | 74
| [継承] |
○号 (必須): | □ | 12
| [継承] |
○頁 (必須): | □ | 1719 1724
| [継承] |
○都市 (任意): |
○年月日 (必須): | □ | 西暦 2003年 12月 初日 (平成 15年 12月 初日)
| [継承] |
○URL (任意): | □ | http://www.joponline.org/doi/abs/10.1902/jop.2003.74.12.1719
| [継承] |
○DOI (任意): | □ | 10.1902/jop.2003.74.12.1719 (→Scopusで検索)
| [継承] |
○PMID (任意): | □ | 14974811 (→Scopusで検索)
| [継承] |
○CRID (任意): |
○WOS (任意): |
○Scopus (任意): |
○評価値 (任意): |
○被引用数 (任意): |
○指導教員 (推奨): |
○備考 (任意): | 1. | (英) Article.Affiliation: Department of Periodontology and Endodontology, Tokushima University School of Dentistry, Tokushima, Japan. (日)
| [継承] |
| 2. | (英) Article.PublicationTypeList.PublicationType: Journal Article (日)
| [継承] |
| 3. | (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't (日)
| [継承] |