Pneumococcal DNA-binding proteins released through autolysis induce the production of proinflammatory cytokines via toll-like receptor 4

• Material Type: 博士論文
• Title: Pneumococcal DNA-binding proteins released through autolysis induce the production of proinflammatory cytokines via toll-like receptor 4
• Author/Editor: Nagai, Kosuke
• Publication, Distribution, etc.: 新潟大学
• Publication Date: 2019-03-25
• Publication Date (W3CDTF): 2019-03-25
• Alternative Title: Pneumococcal DNA-binding proteins released through autolysis induce the production of proinflammatory cytokines via toll-like receptor 4; 自己溶菌に伴い漏出する肺炎球菌のDNA結合タンパク質は，TLR4を介して炎症性サイトカインの産生を促進する
• Degree grantor/type: 新潟大学
• Date Granted: 2019-03-25
• Date Granted (W3CDTF): 2019-03-25
• Dissertation Number: 甲第4568号
• Degree Type: 博士（歯学）
• Conferring No. (Dissertation): 甲第4568号
• Text Language Code: eng
• Subject Heading: Streptococcus pneumoniae; Autolysis; DNA-binding protein; DnaK; EF-Tu; GAPDH; TLR4
• Note (General): Streptococcus pneumoniae is a leading cause of bacterial pneumonia. Our previous study suggested that S.pneumoniae autolysis-dependently releases intracellular pneumolysin, which subsequently leads to lung injury. In this study, we hypothesized that pneumococcal autolysis induces the leakage of additional intracellular molecules that could increase the pathogenicity of S. pneumoniae. Liquid chromatography tandem-mass spectrometry analysis identified that chaperone protein DnaK, elongation factor Tu (EF-Tu), and glyceraldehyde-3- phosphate dehydrogenase (GAPDH) were released with pneumococcal DNA by autolysis. We demonstrated that recombinant (r) DnaK, rEF-Tu, and rGAPDH induced significantly higher levels of interleukin-6 and tumor necrosis factor production in peritoneal macrophages and THP-1-derived macrophage-like cells via toll-like receptor 4. Furthermore, the DNA-binding activity of these proteins was confirmed by surface plasmon resonance assay. We demonstrated that pneumococcal DnaK, EF-Tu, and GAPDH induced the production of proinflammatory cytokines in macrophages, and might cause host tissue damage and affect the development of pneumococcal diseases.; 学位の種類: 博士（歯学）. 報告番号: 甲第4568号. 学位記番号: 新大院博（歯）甲第417号. 学位授与年月日: 平成31年3月25日; Cellular Immunology. 2018, 325, 14-22.; 新大院博（歯）甲第417号; 開始ページ : 14; 終了ページ : 22
• DOI: info:doi/10.1016/j.cellimm.2018.01.006; https://doi.org/info:doi/10.1016/j.cellimm.2018.01.006
• Persistent ID (NDL): info:ndljp/pid/11337470; https://dl.ndl.go.jp/pid/11337470
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2019-08-03T12:23:27+09:00
• Date Created (W3CDTF): 2019-09-10
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
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• Availability of remote photoduplication service: 可
• Periodical Title (URI): http://hdl.handle.net/10191/51346
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp