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研究生:盧育慧
研究生(外文):Yu-Hui Lu
論文名稱:比較SPEA與SPEB在A群鏈球菌感染過程中的角色
論文名稱(外文):Comparison in the roles of SPE A and SPE B during group A streptococcal infections
指導教授:林以行劉清泉劉清泉引用關係
指導教授(外文):Yee-shin LinChing-chuan Liu
學位類別:碩士
校院名稱:國立成功大學
系所名稱:微生物及免疫學研究所
學門:生命科學學門
學類:微生物學類
論文種類:學術論文
論文出版年:2003
畢業學年度:91
語文別:中文
論文頁數:79
中文關鍵詞:A群鏈球菌熱性外毒素A熱性外毒素B
外文關鍵詞:Group A streptococcusSPE ASPE B
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A群鏈球菌的感染會導致人類嚴重的疾病,所造成致死性併發症的臨床症狀包括鏈球菌毒性休克症候群 (STSS)、菌血症及壞死性肌膜炎。有相當廣泛的毒力因子參與A群鏈球菌的致病過程,過去的研究顯示鏈球菌致熱性外毒素B (SPE B),為一半胱氨酸蛋白酶 (cysteine protease),是嚴重的A群鏈球菌感染中重要的致病因子。然而,有研究報告指出一種具有超級抗原特性的鏈球菌致熱性外毒素A (SPE A) 較為重要。speA基因是由噬菌體 (bacteriophage) 攜帶入細菌內,並非所有的毒性休克症候群菌株都有SPE A的表現或帶有speA基因;相對於speA,speB基因是位於染色體上,所有A群鏈球菌都帶有speB基因。為了釐清SPE A與SPE B在A群鏈球菌感染中所扮演的角色,本研究從臨床的檢體與動物感染的模式來做探討。收集自1979~1996年北臺灣台大醫院及1996年至目前南臺灣成大醫院所分離的A群鏈球菌臨床菌株加以分析。所有A群鏈球菌都帶有speB基因,僅28.4%帶有speA基因。在南臺灣成大醫院所分離的菌株中,是否帶有speA基因與疾病嚴重度具統計上的差異,而SPE A蛋白質的表現與疾病的嚴重度間並無相關性;另外,SPE B蛋白質的表現與疾病嚴重度間亦具統計的差異;在蛋白水解酶活性方面,雖有隨疾病嚴重度增加而上升的傾向,但差異並不大。由血清偵測anti-SPE B抗體的濃度,與疾病嚴重度間具相當程度的關連,而anti-SPE A抗體的濃度與疾病嚴重度間的相關性不如anti-SPE B來的顯著。我們同時採用小鼠皮下氣囊感染模式來研究SPE A與SPE B的角色。利用純化的SPE A、SPE B以及不具蛋白水解酶活性的SPE B定點突變株C192S打入已感染speB突變株SW510的小鼠後,比較小鼠存活率,感染部位、血液、器官菌量的計數,氣囊回抽液細胞浸潤的情形,NO的測定及器官的病理變化來探討對細菌致病力的影響。其中,給予SPE B之小鼠在感染48小時後陸續死亡,其死亡率達50%,而給予SPE A及C192S,在感染10天後仍維持100%的存活率。我們計數皮下氣囊感染部位、血液、肝臟、腎臟及脾臟的菌量,與SPE B的給予有關,顯示在感染過程中SPE B除了可以造成細菌持續的感染之外,也可以使細菌由局部的感染侵襲到更深層的組織進而散佈到全身導致菌血症。且感染後24小時,給予SPE B的小鼠皮下氣囊回抽液的浸潤細胞數高於給予SPE A及C192S之小鼠。本研究亦測定皮下氣囊NO的濃度,在24小時後,給予SPE B之小鼠皮下氣囊局部的NO濃度較給予SPE A及C192S為高,NO與A群鏈球菌的感染所引起的發炎與侵襲能力的相關性仍待釐清。給予SPE B的小鼠在感染後24及72小時,皮下、腎臟及肝臟皆發生病變。根據臨床流行病學的分析,可看出在臺灣過去幾年SPE A對A群鏈球菌的感染的角色並不如SPE B來的重要;透過小鼠的動物感染模式,可更進一步證實SPE B角色的重要,印證在臨床的研究結果。
The group A streptococcus (GAS) may cause serious diseases in human. Clinical features that result in life-threatening sequelae of these infections include streptococcal toxic shock syndrome (STSS), bacteremia, and necrotizing fasciitis. GAS have a vast repertoire of virulence factors that participate in pathogenesis. Streptococcal pyrogenic exotoxin B (SPE B), a cysteine protease, has been previously shown to play an important role in severe GAS infections. However, it has also been reported that SPE A, a superantigen, plays a key role. speA is encoded on bacterialphage. Not all strains associated with streptococcal toxic shock syndrome produced SPE A or contained the speA gene. On the contrary, the chromosomally encoded speB gene is carried by every strain of GAS. The involvement of SPE A and SPE B in severe diseases has been controversial in previous studies. In order to dissect the roles played by SPE A and SPE B in GAS infections, studies have been carried out by both analyzing the clinical isolates and using the infectious animal model. We collected GAS clinical isolates from northern Taiwan NTUH during 1979~1996 and from southern Taiwan NCKUH since 1996 to present. All strains of GAS contain the gene for speB, while only 27.8% contain the speA gene. There is significant difference between disease severity and the presence of speA gene in GAS strains from southern Taiwan. However, there is no correlation between in vitro production of SPE A and disease severity. Although higher protease activity was found in more severe clinical isolates, there is no significant difference between protease activity and disease severity. There is significant correlation between levels of anti-SPE B antibodies and disease severity, and less correlation was found between levels of anti-SPE A and disease severity. We further adopt skin air sac as the infection route for studying the roles of SPE A and SPE B in the mouse model. The recombinant SPE A, SPE B or SPE B mutant C192S which lack of protease activity were added in the air pouch after inoculation with speB mutant strain SW510 to compare the mortality rates, bacterial growth and dissemination, cell infiltration, NO production and tissue damage. This study may help to better understand the roles of SPE A and SPE B in the GAS infections. The mice treated with SPE B have higher mortality (50%) than SPE A- and C192S-treated mice. Bacterial numbers in the air pouch exudates, liver, kidney and spleen from SPE B-treated mice were higher than SPE A- and C192S-treated mice 24 hours after infection. Results showed that SPE B may facilitate bacterial dissemination and invasion during GAS infection. The infiltrated cell numbers and the levels of nitric oxide (NO) in the air pouch exudates of SPE B-treated mice were higher than SPE A- and C192S-treated mice 24 hours after bacterial inoculation. The role of NO during bacterial invasion remains to be clarified. The histopathological changes in various organs were examined showing lesions in subcutaneous, kidney and liver in SPE B-treated mice at 24 and 72 hours. Taken together, the epidemiological studies indicate that SPE A plays a less important role than SPE B in Taiwan. Studies in the animal model further confirms that SPE B plays an important role in GAS infections.
中文摘要I
英文摘要III
誌謝V
目錄VI
表目錄VIII
圖目錄IX
縮寫檢索表XI

緒論1
材料與方法
一、實驗菌株與質体6
二、儀器與藥品6
三、細菌及細胞的培養與保存6
四、重組DNA之製備7
五、SPE A重組蛋白的表現及純化11
六、蛋白質電泳及西方墨點分析12
七、SPE A刺激細胞增生的作用14
八、SPE B及其突變株重組蛋白的表現及純化14
九、蛋白水解酶活性分析 (Protease assay)14
十、SPE A多株抗體的製備15
十一、SPE A單株抗體的製備15
十二、利用ELISA測定細菌上清液中SPE A的含量18
十三、A群鏈球菌之小鼠感染模式20
結果
一、speA重組基因的製備23
二、SPE A重組蛋白的製備23
三、單株抗體的製備24
四、SPE A刺激細胞增生的作用24
五、Pro SPE B及其突變株重組蛋白的製備24
六、分析臺灣A群鏈球菌感染的臨床菌株及病人血清表現之差異24
A群鏈球菌之小鼠感染模式27
討論
分析臺灣A群鏈球菌感染的嚴重度與致病因子的相關性31
A群鏈球菌之小鼠感染模式33
參考文獻37
表43
圖53
附錄71
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