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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
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dc.contributor.advisor | 許秉寧(Ping-Ning Hsu) | |
dc.contributor.author | Chang-Wei Chen | en |
dc.contributor.author | 陳昶瑋 | zh_TW |
dc.date.accessioned | 2021-06-15T01:20:03Z | - |
dc.date.available | 2012-09-15 | |
dc.date.copyright | 2009-09-15 | |
dc.date.issued | 2009 | |
dc.date.submitted | 2009-07-26 | |
dc.identifier.citation | Ahmad, A., Govil, Y., and Frank, B.B. (2003). Gastric mucosa-associated lymphoid tissue lymphoma. Am J Gastroenterol 98, 975-986.
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dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/42696 | - |
dc.description.abstract | 胃幽門螺旋桿菌(Helicobacter pylori)在分類上屬於革蘭氏陰性菌,感染胃幽門螺旋桿菌會造成胃炎、胃潰瘍、十二指腸潰瘍、胃線癌以及胃黏膜相關淋巴組織淋巴瘤。胃幽門螺旋桿菌致病因子CagA 是分子量120~148 kD 的蛋白質,可經由第四型分泌系統(type IV secretion system)注入細胞內。進入細胞的CagA 會被宿主細胞內的蛋白質磷酸酶所磷酸化。而磷酸化CagA 與SHP-2 結合後可活化ERK 訊息傳遞途徑。在CagA+胃幽門螺旋桿菌菌株已被發現經由刺激cyclin D1 的表現,進而影響宿主細胞的細胞週期與生存。研究指出在胃上皮細胞中CagA 可以活化STAT3。在B 細胞活化及分化中STAT3 扮演重要角色。為了研究胃幽門螺旋桿菌調控B 細胞轉型的機制,我們假設胃幽門螺旋桿菌所表現的CagA 可能扮演重要的角色。第一步我們利用胃幽門螺旋桿菌與BJAB 細胞共同培養的系統,發現胃幽門螺旋桿菌能直接將CagA 送入B 細胞中。為了進一步探討胃幽門螺旋桿菌是否透過CagA 直接影響B 細胞的活化,我們觀察CagA 對B 細胞活化分子STAT3 與P38 的影響,結果顯示胃幽門螺旋桿菌可活化STAT3 與P38 途徑,然而在cagA 基因剔除菌株中磷酸化STAT3與磷酸化P38 表現量下降,因此在胃幽門螺旋桿菌影響B 細胞活化中,CagA可以增加STAT3 與P38 活化。接著我們探討送入B 細胞中的CagA 是否會影響B cell 存活。我們發現胃幽門螺旋桿菌可以使Bcl-2 和Bcl-XL 表現上升,Mcl-1不受影響,但是在剔除cagA 基因後,Bcl-2 和Bcl-XL 表現上升就被抑制,顯示胃幽門螺旋桿菌CagA 可以增加B 細胞存活。將CagA 送入B 細胞可以觀察到Bcl-2 和Bcl-XL 表現上升。此外在B 細胞分化上,我們也觀察到胃幽門螺旋桿菌可使B 細胞內Bcl-6 蛋白質表現量下降,然而在剔除cagA 基因的菌株中,
Bcl-6 並無明顯下降。利用real-time PCR 測量BCL-6 mRNA 表現,也發現BCL-6mRNA 表現受到抑制,但是在cagA 基因剔除菌株共同培養的組別並未發現相同結果。與漿細胞分化相關的轉錄分子Blimp-1,利用real-time PCR 我們也觀察到Blimp-1 mRNA 表現上升。為了了解活化的STAT3 在誘導Bcl-2 和Bcl-XL表現的機制,我們利用JAK 抑制劑抑制STAT3 途徑活化與STAT3 siRNA 抑制STAT3 表現來觀察Bcl-2 和Bcl-XL 表現。我們發現Bcl-2 和Bcl-XL 表現會被抑制。但是抑制STAT3 表現後,Bcl-6 及Blimp-1 並未受到影響。這些結果顯示CagA 被胃幽門螺旋桿菌送入B 細胞可以活化STAT3 途徑,進而使Bcl-2 和Bcl-XL 表現上升。這些抗細胞凋亡分子的表現可能參與胃幽門螺旋桿菌造成胃黏膜相關淋巴組織淋巴瘤的形成機制之一。阻斷CagA 進入細胞或是抑制CagA細胞內活性,在治療上可能是新的研究方向。 | zh_TW |
dc.description.abstract | Helicobacter pylori is a gram-negative bacteria. Human who infected Helicobacter pylori causes chronic gastrits, peptic ulcer and gastric adenocarcinoma. CagA, Helicobacter pylori virulent factor, is 120~148 kD. It is translocated into the cell by type IV secretion system. In host cells, CagA is phosphorylated by protein kinase. Phospho-CagA binds SHP-2 to activate ERK signal pathway. cagA+ H. pylori strains have been reported to affect the cell cycle by stimulating cyclin D1 expression and host cell survival. In previous studies, CagA activates STAT3 pathway in gastric epithelium cell. In B cell activation and differentiation, STAT3 also plays an important role. To study the mechanism of Helicobacter pylori-dependent regulation of B cell transformation, we suggest that Helicobacter pylori CagA may play an important role. First, we found that H. pylori translocates CagA into B cell in H. pylori and BJAB cell co-culture system. To further examine whether H. pylori directly regulates B cell activation via CagA, we investigate the phosphorylation of B cell activation molecule STAT3 and P38. Our results show that H. pylori activates STAT3 and P38 pathway, but the expression of phospho-STAT3 and phospho-P38 decrease when BJAB cell co-cultures with cagA knock-out strain. Therefore, CagA increases STAT3 and P38 activation in B cell activation. Next, we explore whether CagA in B cells regulates B cell survival. We found that H. pylori induces Bcl-2 and Bcl-XL expression, but Bcl-2 and Bcl-XL expression is not up-regulated when BJAB cell co-cultures with cagA knock-out H. pylori strain. We transfected CagA into B cell and found that Bcl-2 and Bcl-XL expression is up-regulated. The results indicate that H. pylori CagA can increase B cell survival. Moreover, in B cell differentiation, we also found that H. pylori decreases Bcl-6 protein expression, but Bcl-6 does not decrease when BJAB cell co-cultures with cagA knock-out strain. We used real-time PCR to investigate Bcl-6 mRNA expression. The results show that expression of
Bcl-6 mRNA is inhibited, but we do not found the same result when BJAB cell co-cultures with cagA knock-out strain. We used real-time PCR to explore whether H. pylori can affect the expression of plasma cell differentiation associated molecule Blimp-1. Our results show that the H. pylori increases expression of Blimp-1 mRNA. To investigate the role of activated STAT3 in the mechanism of induction of Bcl-2 and Bcl-XL expression, we used Jak inhibitor AG490 to inhibit STAT3 pathway and STAT3 siRNA to inhibit STAT3 expression. Our results show that Bcl-2 and Bcl-XL expression is inhibited. However, inhibition of STAT3 expression does not regulate Bcl-6 and Blimp-1 expression. These results demonstrate that H. pylori translocate CagA into B cells to induce Bcl-2 and Bcl-XL expression via STAT3 pathway and to modulate Bcl-6 and Blimp-1 expression. These anti-apoptotic molecules induced by CagA might be one of the mechanisms that Helicobacter pylori controls B cell transformation, and that indicate that inhibition of translocating CagA into B cell or inhibition of CagA activity in B cell might be new way to cure the MALTlymphoma. | en |
dc.description.provenance | Made available in DSpace on 2021-06-15T01:20:03Z (GMT). No. of bitstreams: 1 ntu-98-R96449008-1.pdf: 2008479 bytes, checksum: bd8402b9358bde2ba3f3961daf1e5ef9 (MD5) Previous issue date: 2009 | en |
dc.description.tableofcontents | 誌謝 ii
中文摘要 iii Abstract v 研究背景 1 1 胃幽門螺旋桿菌與致病性之簡介 1 2 CagA 2 3 STAT3 3 4 Bcl-6、Blimp-1 4 材料與方法 7 1 實驗材料 7 2 實驗方法 12 實驗結果 14 1 CagA 可被胃幽門螺旋桿菌送入B 細胞 14 2 胃幽門螺旋桿菌藉由CagA 活化STAT3 與MAPK 訊息途徑 14 3 胃幽門螺旋桿菌藉由CagA 誘導Bcl-2 與Bcl-XL 表現 15 4 胃幽門螺旋桿菌透過STAT3 途徑調控Bcl-2 與Bcl-XL 16 5 胃幽門螺旋桿菌藉由CagA 誘導Blimp-1 表現上升,降低Bcl-6 表現 16 結果討論 18 1 胃幽門螺旋桿菌可以將CagA 送入B 細胞 18 2 胃幽門螺旋桿菌透過CagA 影響B 細胞的活化與存活 18 3 STAT3 在胃幽門螺旋桿菌透過CagA 影響Bcl-2 及Bcl-XL 表現扮演之角色 20 4 胃幽門螺旋桿菌透過CagA 影響B 細胞分化相關轉錄因子表現 20 5 結論 21 參考文獻 23 圖表說明 34 | |
dc.language.iso | zh-TW | |
dc.title | 胃幽門螺旋桿菌CagA調控Bcl-6、Blimp-1以及抗細胞凋亡分子Bcl-2 和 Bcl-XL之研究 | zh_TW |
dc.title | Helicobacter pylori CagA in regulation of Bcl-6, Blimp-1, and anti-apoptotic molecules Bcl-2 and Bcl-XL | en |
dc.type | Thesis | |
dc.date.schoolyear | 97-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 司徒惠康(Huey-Kang Sytwu),林國儀(Kuo-I Lin) | |
dc.subject.keyword | 胃幽門螺旋桿菌,B細胞,胃黏膜相關淋巴組織淋巴瘤,Bcl-2,Bcl-XL,STAT3,CagA,Bcl-6,Blimp-1, | zh_TW |
dc.subject.keyword | Helicobacter pylori,gastric MALT lymphoma,B cell,Bcl-2,Bcl-XL,STAT3,CagA,Bcl-6,Blimp-1, | en |
dc.relation.page | 41 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2009-07-27 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 免疫學研究所 | zh_TW |
顯示於系所單位: | 免疫學研究所 |
文件中的檔案:
檔案 | 大小 | 格式 | |
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ntu-98-1.pdf 目前未授權公開取用 | 1.96 MB | Adobe PDF |
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