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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 賈景山(Jean-San Chia) | |
dc.contributor.author | Ya-Hsin Chen | en |
dc.contributor.author | 陳雅昕 | zh_TW |
dc.date.accessioned | 2021-06-17T04:37:24Z | - |
dc.date.available | 2021-08-30 | |
dc.date.copyright | 2018-08-30 | |
dc.date.issued | 2018 | |
dc.date.submitted | 2018-08-08 | |
dc.identifier.citation | 1. Nakano, K. and T. Ooshima, Serotype classification of Streptococcus mutans and its detection outside the oral cavity. Future Microbiol, 2009. 4(7): p. 891-902.
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Jung, C.J., et al., Streptococcus mutans autolysin AtlA is a fibronectin-binding protein and contributes to bacterial survival in the bloodstream and virulence for infective endocarditis. Mol Microbiol, 2009. 74(4): p. 888-902. 28. Yoshimura, G., et al., Identification and molecular characterization of an N-Acetylmuraminidase, Aml, involved in Streptococcus mutans cell separation. Microbiol Immunol, 2006. 50(9): p. 729-42. 29. Rogers, H.J., H.R. Perkins, and J.B. Ward, The bacterial autolysins, in Microbial Cell Walls and Membranes, H.J. Rogers, H.R. Perkins, and J.B. Ward, Editors. 1980, Springer Netherlands: Dordrecht. p. 437-460. 30. Shockman, G.D. and J.V. Höltje, Chapter 7 Microbial peptidoglycan (murein) hydrolases, in New Comprehensive Biochemistry, J.M. Ghuysen and R. Hakenbeck, Editors. 1994, Elsevier. p. 131-166. 31. Nombela, C. and F.o.E.M. Societies, Microbial cell wall synthesis and autolysis: proceedings of a symposium sponsored by the Federation of European Microbiological Societies held in Madrid (Spain) on July 3rd-6th, 1984. 1984: Elsevier Science Publishers. 32. Mani, N., et al., Autolysis-defective mutant of Staphylococcus aureus: pathological considerations, genetic mapping, and electron microscopic studies. Infect Immun, 1994. 62(4): p. 1406-9. 33. Shibata, Y., et al., Identification and characterization of an autolysin-encoding gene of Streptococcus mutans. Infect Immun, 2005. 73(6): p. 3512-20. 34. Ahn, S.J. and R.A. Burne, The atlA operon of Streptococcus mutans: role in autolysin maturation and cell surface biogenesis. J Bacteriol, 2006. 188(19): p. 6877-88. 35. Ahn, S.J. and R.A. Burne, Effects of oxygen on biofilm formation and the AtlA autolysin of Streptococcus mutans. J Bacteriol, 2007. 189(17): p. 6293-302. 36. Jung, C.J., et al., AtlA Mediates Extracellular DNA Release, Which Contributes to Streptococcus mutans Biofilm Formation in an Experimental Rat Model of Infective Endocarditis. Infect Immun, 2017. 85(9). 37. Santoro, J. and M.E. Levison, Rat model of experimental endocarditis. Infect Immun, 1978. 19(3): p. 915-8. 38. Nakano, K., et al., Serotype distribution of Streptococcus mutans a pathogen of dental caries in cardiovascular specimens from Japanese patients. J Med Microbiol, 2007. 56(Pt 4): p. 551-6. 39. Nakano, K., et al., Detection of oral bacteria in cardiovascular specimens. Oral Microbiol Immunol, 2009. 24(1): p. 64-8. 40. Lu, T., et al., Phagocytosis and killing of Staphylococcus aureus by human neutrophils. J Innate Immun, 2014. 6(5): p. 639-49. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/70758 | - |
dc.description.abstract | 感染性心膜炎(Infective endocarditis, IE)為一種具有高復發率以及死亡率的心血管感染疾病。轉糖鏈球菌(Streptococcus mutans)屬於草綠色鏈球菌(viridans streptococci),是口腔內的正常菌叢,也是引起感染性心內膜炎的主要致病菌之一。逃避宿主免疫監控以及生物膜形成是細菌引起感染性心內膜炎的兩大毒性因子。我們先前的研究顯示,S. mutans所產生的一種蛋白AtlA,可以透過結合血漿中的纖維蛋白(fibronectin)來增強細菌對於嗜中性白血球殺菌的抵抗能力,同時AtlA也能夠藉由調控細胞外 DNA(extracellular DNA, eDNA)的釋放,以促進細菌在心臟瓣膜上形成生物膜的能力。有趣的是,我們透過針對AtlA的多株抗體辨認到了一種AtlA的相似蛋白,並將之命名為Ahp。因此,我們假設Ahp也可能在S. mutans中發揮與AtlA類似的作用,在生物膜形成與免疫逃避中扮演重要的角色。利用實驗性心內膜炎的老鼠模型,我們證明了Ahp在感染性心內膜炎的致病機制中具有重要的作用,並且在體外實驗中,顯示Ahp主要的功能在於幫助細菌逃避嗜中性白血球的胞殺作用。更有趣的是,我們發現S. mutans可根據Ahp的完整性分為兩類,當原本表現截短形式Ahp的菌株UA159表達完整的形式時,此菌株引起感染性心內膜炎的致病能力將顯著增加。從臨床血液檢體分離出的S. mutans菌株中,具有完整形式Ahp的臨床菌株也表現出更高的逃避免疫攻擊及引起感染性心內膜炎的能力。這些結果證明Ahp能夠幫助S. mutans逃避嗜中性白血球的胞殺作用,有助於細菌引發感染性心內膜炎的致病能力。 | zh_TW |
dc.description.abstract | Infective endocarditis (IE) is an infectious disease of the cardiovascular system, and carries a high recurrence and mortality rate. Streptococcus mutans, a member of viridans streptococci, is a commensal in the oral cavity and also one of major opportunistic pathogen for causing IE. Escaping immune surveillance and forming biofilm are two determining virulent factors for bacteria to cause IE. Our previous reports demonstrated that one S. mutans protein, AtlA, not only plays the role in enhancing bacterial resistance against neutrophil killing through binding fibronectin in the plasma, but also contributes to bacterial biofilm formation on the heart valve through mediating extracellular DNA release. Interestingly, we identified a AtlA homologous protein (named Ahp) by using polyclonal antibodies against AtlA. Therefore, we hypothesized Ahp may also play similar roles in modulating S. mutans virulence in biofilm formation and immune evasion. By using in vivo rat experimental IE model, we demonstrated the role of Ahp in the pathogenesis of IE. In vitro assays showed that Ahp majorly plays role in mediating bacterial ability to escape neutrophil killing. More interestingly, we found that S. mutans strains can be grouped into two types according to the intactness of Ahp. When the strain UA159, which originally exhibits the truncated form of Ahp, expresses the intact Ahp, its virulence for causing IE will be dramatically increased. The clinical blood isolates of S. mutans with the intact form of Ahp also exhibit higher abilities to escape immune surveillance and cause IE. These data suggested that Ahp mediates S. mutans to escape neutrophil killing, which contributes to the pathogenesis of IE. | en |
dc.description.provenance | Made available in DSpace on 2021-06-17T04:37:24Z (GMT). No. of bitstreams: 1 ntu-107-R05450015-1.pdf: 3878139 bytes, checksum: 27c247ac76a45d30a2b6c35c4e3517d2 (MD5) Previous issue date: 2018 | en |
dc.description.tableofcontents | 口試委員審定書 i
誌謝 ii 中文摘要 iii 英文摘要 iv 目錄 v 圖目錄 x 表目錄 xi 第一章 緒論 1 1.1 轉糖鏈球菌(Streptococcus mutans) 1 1.2 感染性心內膜炎 1 1.3 轉糖鏈球菌引起心內膜炎的相關毒性因子 3 1.4 轉糖鏈球菌的自體溶體素(AtlA) 3 1.5 研究目的與實驗設計 5 第二章 實驗材料與方法 6 2.1 實驗材料 6 2.2 實驗方法 6 2.2.1 實驗性心內膜炎的老鼠模型 6 2.2.2 細菌處理與感染老鼠之方法 6 2.2.3 檢體處理與細菌培養 7 2.2.4 生物膜形成能力測定 7 2.2.5 全血殺菌實驗(Whole blood killing assay) 7 2.2.6 測定小鼠循環系統中的細菌存活率 8 2.2.7 嗜中性白血球之分離技術 8 2.2.8 嗜中性白血球殺菌實驗 9 2.2.9 過氧化氫殺菌實驗 9 2.2.10 西方墨點法 9 第三章 結果 11 3.1 Ahp的缺失會顯著影響轉糖鏈球菌於心內膜炎的致病能力 11 3.2 Ahp參與轉糖鏈球菌逃避宿主免疫細胞的過程 11 3.3 Ahp在GS-5及UA159中具有不同的大小 11 3.4 完整的Ahp使UA159提升在感染性心內膜炎中的致病能力 12 3.5 完整的Ahp幫助轉糖鏈球菌提升在血液中的存活率 12 3.6 Ahp可幫助轉糖鏈球菌抵抗嗜中性白血球的殺菌作用 13 3.7 臨床菌株的Ahp分析及毒性分析 13 第四章 討論 15 4.1 Ahp表現的缺失影響轉糖鏈球菌在感染性心內膜炎中的致病能力 15 4.2 Ahp的完整性影響轉糖鏈球菌的致病能力 15 4.3 轉糖鏈球菌臨床菌株Ahp的差異對細菌毒性的影響 16 參考文獻 18 附錄 22 | |
dc.language.iso | zh-TW | |
dc.title | 轉糖鏈球菌之自體溶體素相似蛋白在感染性心內膜炎中所扮演的角色 | zh_TW |
dc.title | Role of Ahp in Streptococcus mutans-induced infective endocarditis | en |
dc.type | Thesis | |
dc.date.schoolyear | 106-2 | |
dc.description.degree | 碩士 | |
dc.contributor.coadvisor | 鍾筱菁(Chiau-Jing Jung) | |
dc.contributor.oralexamcommittee | 鄧麗珍(Lee-Jene Teng) | |
dc.subject.keyword | 轉糖鏈球菌,感染性心內膜炎,自體溶體素相似蛋白,吞噬作用,嗜中性白血球, | zh_TW |
dc.subject.keyword | Streptococcus mutans,Infective endocarditis,AtlA homologous protein,Phagocytosis,Neutrophil, | en |
dc.relation.page | 36 | |
dc.identifier.doi | 10.6342/NTU201802681 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2018-08-08 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 口腔生物科學研究所 | zh_TW |
顯示於系所單位: | 口腔生物科學研究所 |
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