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Host-dependent Lewis (Le) antigen expression in Helicobacter pylori cells recovered from Leb-transgenic mice.从 Leb 转基因小鼠中回收的幽门螺杆菌细胞中宿主依赖性 Lewis(Le)抗原表达。
J Exp Med. 2009 Dec 21;206(13):3061-72. doi: 10.1084/jem.20090683. Epub 2009 Dec 14.
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Helicobacter pylori type IV secretion apparatus exploits beta1 integrin in a novel RGD-independent manner.幽门螺杆菌 IV 型分泌装置以一种新型的非 RGDI 依赖性方式利用β1 整合素。
PLoS Pathog. 2009 Dec;5(12):e1000684. doi: 10.1371/journal.ppat.1000684. Epub 2009 Dec 4.
3
Can Helicobacter pylori invade human gastric mucosa?: an in vivo study using electron microscopy, immunohistochemical methods, and real-time polymerase chain reaction.幽门螺杆菌能否侵犯人类胃黏膜?——一项应用电子显微镜、免疫组织化学方法和实时聚合酶链反应的体内研究。
J Clin Gastroenterol. 2010 Jul;44(6):416-22. doi: 10.1097/MCG.0b013e3181c21c69.
4
Bacterial membrane vesicles deliver peptidoglycan to NOD1 in epithelial cells.细菌膜泡将肽聚糖递呈给上皮细胞中的 NOD1。
Cell Microbiol. 2010 Mar;12(3):372-85. doi: 10.1111/j.1462-5822.2009.01404.x. Epub 2009 Nov 2.
5
Helicobacter pylori counteracts the apoptotic action of its VacA toxin by injecting the CagA protein into gastric epithelial cells.幽门螺杆菌通过将CagA蛋白注入胃上皮细胞来对抗其VacA毒素的凋亡作用。
PLoS Pathog. 2009 Oct;5(10):e1000603. doi: 10.1371/journal.ppat.1000603. Epub 2009 Oct 2.
6
Response of gastric epithelial progenitors to Helicobacter pylori Isolates obtained from Swedish patients with chronic atrophic gastritis.胃上皮祖细胞对从瑞典慢性萎缩性胃炎患者分离出的幽门螺杆菌的反应
J Biol Chem. 2009 Oct 30;284(44):30383-94. doi: 10.1074/jbc.M109.052738. Epub 2009 Sep 1.
7
Protease-activated receptor-1 down-regulates the murine inflammatory and humoral response to Helicobacter pylori.蛋白酶激活受体-1下调幽门螺杆菌诱导的小鼠炎症和体液免疫反应。
Gastroenterology. 2010 Feb;138(2):573-82. doi: 10.1053/j.gastro.2009.08.043. Epub 2009 Aug 23.
8
Inhibition of heat shock protein expression by Helicobacter pylori.幽门螺杆菌对热休克蛋白表达的抑制作用。
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Role of partitioning-defective 1/microtubule affinity-regulating kinases in the morphogenetic activity of Helicobacter pylori CagA.分选缺陷蛋白1/微管亲和调节激酶在幽门螺杆菌CagA形态发生活性中的作用
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10
Role of Helicobacter pylori CagA molecular variations in induction of host phenotypes with carcinogenic potential.幽门螺杆菌细胞毒素相关基因A(CagA)分子变异在诱导具有致癌潜力的宿主表型中的作用。
J Infect Dis. 2009 Apr 15;199(8):1218-21. doi: 10.1086/597416.

幽门螺杆菌对人类宿主的隐秘操控。

Surreptitious manipulation of the human host by Helicobacter pylori.

作者信息

Israel Dawn A, Peek Richard M

机构信息

Department of Medicine; Division of Gastroenterology, Nashville, TN USA.

出版信息

Gut Microbes. 2010 Mar;1(2):119-127. doi: 10.4161/gmic.1.2.11991.

DOI:10.4161/gmic.1.2.11991
PMID:20976041
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2958064/
Abstract

Microbial pathogens contribute to the development of more than 1 million cases of cancer per year. Gastric adenocarcinoma is the second leading cause of cancer-related death in the world, and gastritis induced by Helicobacter pylori is the strongest known risk factor for this malignancy. H. pylori colonizes the stomach for years, not days or weeks, as is usually the case for bacterial pathogens and it always induces inflammation; however, only a fraction of colonized individuals ever develop disease. Identification of mechanisms through which H. pylori co-opts host defenses to facilitate its own persistence will not only improve diagnostic and therapeutic modalities, but may also provide insights into other diseases that arise within the context of long-term pathogen-initiated inflammatory states, such as chronic viral hepatitis and hepatocellular carcinoma.

摘要

微生物病原体每年导致超过100万例癌症的发生。胃腺癌是全球癌症相关死亡的第二大主要原因,而幽门螺杆菌引起的胃炎是已知的这种恶性肿瘤最强的危险因素。幽门螺杆菌在胃中定植数年,而不像通常的细菌病原体那样仅定植数天或数周,并且它总是引发炎症;然而,只有一小部分被定植的个体最终会发病。确定幽门螺杆菌利用宿主防御机制以促进自身持续存在的机制,不仅将改善诊断和治疗方式,还可能为在长期病原体引发的炎症状态下出现的其他疾病提供见解,例如慢性病毒性肝炎和肝细胞癌。