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本文引用的文献

1
Helicobacter pylori exploits host membrane phosphatidylserine for delivery, localization, and pathophysiological action of the CagA oncoprotein.幽门螺杆菌利用宿主膜磷脂酰丝氨酸来实现 CagA 癌蛋白的传递、定位和病理生理作用。
Cell Host Microbe. 2010 May 20;7(5):399-411. doi: 10.1016/j.chom.2010.04.005.
2
NOD1 contributes to mouse host defense against Helicobacter pylori via induction of type I IFN and activation of the ISGF3 signaling pathway.NOD1 通过诱导 I 型 IFN 和激活 ISGF3 信号通路促进小鼠宿主抵抗幽门螺杆菌。
J Clin Invest. 2010 May;120(5):1645-62. doi: 10.1172/JCI39481. Epub 2010 Apr 12.
3
Arginase II restricts host defense to Helicobacter pylori by attenuating inducible nitric oxide synthase translation in macrophages.精氨酸酶 II 通过减弱巨噬细胞中诱导型一氧化氮合酶的翻译来限制宿主对幽门螺杆菌的防御。
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4
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。
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5
Helicobacter pylori CagA inhibits PAR1-MARK family kinases by mimicking host substrates.幽门螺杆菌 CagA 通过模拟宿主底物来抑制 PAR1-MARK 家族激酶。
Nat Struct Mol Biol. 2010 Jan;17(1):130-2. doi: 10.1038/nsmb.1705. Epub 2009 Dec 6.
6
Helicobacter pylori immune escape is mediated by dendritic cell-induced Treg skewing and Th17 suppression in mice.幽门螺杆菌免疫逃逸是由树突状细胞诱导的 Treg 偏倚和 Th17 抑制介导的。
Gastroenterology. 2010 Mar;138(3):1046-54. doi: 10.1053/j.gastro.2009.11.043. Epub 2009 Nov 18.
7
Interleukin-1beta promotes gastric atrophy through suppression of Sonic Hedgehog.白细胞介素-1β通过抑制 Sonic Hedgehog 促进胃萎缩。
Gastroenterology. 2010 Feb;138(2):562-72, 572.e1-2. doi: 10.1053/j.gastro.2009.10.043. Epub 2009 Oct 31.
8
Helicobacter pylori dupA gene is not associated with clinical outcomes in the Japanese population.在日本人群中,幽门螺杆菌 dupA 基因与临床结局无关。
Clin Microbiol Infect. 2010 Aug;16(8):1264-9. doi: 10.1111/j.1469-0691.2009.03081.x. Epub 2009 Oct 14.
9
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.
10
Multiple gene status in Helicobacter pylori strains and risk of gastric cancer development.幽门螺杆菌菌株的多种基因状态与胃癌发展风险。
Digestion. 2009;80(3):200-7. doi: 10.1159/000229774. Epub 2009 Sep 15.

幽门螺杆菌和胃癌:调节疾病风险的因素。

Helicobacter pylori and gastric cancer: factors that modulate disease risk.

机构信息

Division of Gastroenterology, Vanderbilt University School of Medicine, 2215 Garland Ave., 1030C MRB IV, Nashville, TN 37232-2279, USA.

出版信息

Clin Microbiol Rev. 2010 Oct;23(4):713-39. doi: 10.1128/CMR.00011-10.

DOI:10.1128/CMR.00011-10
PMID:20930071
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2952980/
Abstract

Helicobacter pylori is a gastric pathogen that colonizes approximately 50% of the world's population. Infection with H. pylori causes chronic inflammation and significantly increases the risk of developing duodenal and gastric ulcer disease and gastric cancer. Infection with H. pylori is the strongest known risk factor for gastric cancer, which is the second leading cause of cancer-related deaths worldwide. Once H. pylori colonizes the gastric environment, it persists for the lifetime of the host, suggesting that the host immune response is ineffective in clearing this bacterium. In this review, we discuss the host immune response and examine other host factors that increase the pathogenic potential of this bacterium, including host polymorphisms, alterations to the apical-junctional complex, and the effects of environmental factors. In addition to host effects and responses, H. pylori strains are genetically diverse. We discuss the main virulence determinants in H. pylori strains and the correlation between these and the diverse clinical outcomes following H. pylori infection. Since H. pylori inhibits the gastric epithelium of half of the world, it is crucial that we continue to gain understanding of host and microbial factors that increase the risk of developing more severe clinical outcomes.

摘要

幽门螺杆菌是一种胃部病原体,大约有 50%的世界人口受到其感染。感染幽门螺杆菌会导致慢性炎症,并显著增加十二指肠和胃溃疡病以及胃癌的发病风险。感染幽门螺杆菌是已知的导致胃癌的最强危险因素,而胃癌是全球癌症相关死亡的第二大主要原因。一旦幽门螺杆菌在胃部环境中定植,它将在宿主的整个生命周期中持续存在,这表明宿主的免疫反应无法有效清除这种细菌。在这篇综述中,我们讨论了宿主的免疫反应,并研究了其他增加这种细菌致病潜力的宿主因素,包括宿主多态性、顶-连接复合体的改变以及环境因素的影响。除了宿主的作用和反应外,幽门螺杆菌菌株具有遗传多样性。我们讨论了幽门螺杆菌菌株中的主要毒力决定因素,以及这些因素与感染幽门螺杆菌后不同的临床结果之间的相关性。由于幽门螺杆菌抑制了世界上一半人口的胃上皮细胞,因此我们必须继续深入了解增加发生更严重临床结果风险的宿主和微生物因素。