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本文引用的文献

1
In vitro suppression of dendritic cells by Helicobacter pylori OipA.幽门螺杆菌OipA对树突状细胞的体外抑制作用
Helicobacter. 2014 Apr;19(2):136-43. doi: 10.1111/hel.12107. Epub 2014 Feb 5.
2
Flow cytometry-based enrichment for cell shape mutants identifies multiple genes that influence Helicobacter pylori morphology.基于流式细胞术的细胞形态突变体富集鉴定出多个影响幽门螺杆菌形态的基因。
Mol Microbiol. 2013 Nov;90(4):869-83. doi: 10.1111/mmi.12405. Epub 2013 Oct 16.
3
Are Lewis b and H type 1 on Helicobacter pylori involved in binding of bacteria to MUC1 mucin?幽门螺杆菌的 Lewis b 和 H 型 1 是否参与细菌与 MUC1 粘蛋白的结合?
Adv Clin Exp Med. 2013 May-Jun;22(3):347-53.
4
Survival in hostile territory: the microbiota of the stomach.在恶劣环境中生存:胃中的微生物组。
FEMS Microbiol Rev. 2013 Sep;37(5):736-61. doi: 10.1111/1574-6976.12027. Epub 2013 Jul 22.
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Designing a dynamic dissolution method: a review of instrumental options and corresponding physiology of stomach and small intestine.设计动态溶出方法:仪器选择及相应的胃和小肠生理学综述。
J Pharm Sci. 2013 Sep;102(9):2995-3017. doi: 10.1002/jps.23494. Epub 2013 Mar 12.
6
Helicobacter pylori γ-glutamyl transpeptidase and vacuolating cytotoxin promote gastric persistence and immune tolerance.幽门螺杆菌 γ-谷氨酰转肽酶和空泡细胞毒素促进胃的持续存在和免疫耐受。
Proc Natl Acad Sci U S A. 2013 Feb 19;110(8):3047-52. doi: 10.1073/pnas.1211248110. Epub 2013 Feb 4.
7
In vivo sequence variation in HopZ, a phase-variable outer membrane protein of Helicobacter pylori.幽门螺杆菌外膜蛋白 HopZ 的体内序列变异。
Infect Immun. 2012 Dec;80(12):4364-73. doi: 10.1128/IAI.00977-12. Epub 2012 Oct 1.
8
Toll-like receptor 9 signaling has anti-inflammatory effects on the early phase of Helicobacter pylori-induced gastritis.Toll 样受体 9 信号通路对幽门螺杆菌诱导的胃炎早期阶段具有抗炎作用。
Biochem Biophys Res Commun. 2012 Sep 28;426(3):342-9. doi: 10.1016/j.bbrc.2012.08.080. Epub 2012 Aug 24.
9
Caspase-1 has both proinflammatory and regulatory properties in Helicobacter infections, which are differentially mediated by its substrates IL-1β and IL-18.半胱天冬酶-1 在幽门螺杆菌感染中具有促炎和调节作用,其底物白细胞介素-1β和白细胞介素-18 通过不同的机制介导。
J Immunol. 2012 Apr 15;188(8):3594-602. doi: 10.4049/jimmunol.1103212. Epub 2012 Mar 7.
10
Helicobacter pylori versus the host: remodeling of the bacterial outer membrane is required for survival in the gastric mucosa.幽门螺杆菌与宿主:细菌外膜的重塑是其在胃黏膜中存活所必需的。
PLoS Pathog. 2011 Dec;7(12):e1002454. doi: 10.1371/journal.ppat.1002454. Epub 2011 Dec 22.

幽门螺杆菌:人类胃微环境中初始阶段及持续定植的细菌策略

Helicobacter pylori: bacterial strategy for incipient stage and persistent colonization in human gastric niches.

作者信息

Rhee Kwang-Ho, Park Jin-Sik, Cho Myung-Je

机构信息

Department of Microbiology, Gyeongsang National University College of Medicine, Research Institute of Life Science, Gyeongsang National University, Jinju, Korea.

出版信息

Yonsei Med J. 2014 Nov;55(6):1453-66. doi: 10.3349/ymj.2014.55.6.1453.

DOI:10.3349/ymj.2014.55.6.1453
PMID:25323880
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4205683/
Abstract

Helicobacter pylori (H. pylori) undergoes decades long colonization of the gastric mucosa of half the population in the world to produce acute and chronic gastritis at the beginning of infection, progressing to more severe disorders, including peptic ulcer disease and gastric cancer. Prolonged carriage of H. pylori is the most crucial factor for the pathogenesis of gastric maladies. Bacterial persistence in the gastric mucosa depends on bacterial factors as well as host factors. Herein, the host and bacterial components responsible for the incipient stages of H. pylori infection are reviewed and discussed. Bacterial adhesion and adaptation is presented to explain the persistence of H. pylori colonization in the gastric mucosa, in which bacterial evasion of host defense systems and genomic diversity are included.

摘要

幽门螺杆菌(H. pylori)在世界上一半人口的胃黏膜中进行长达数十年的定植,在感染初期会引发急性和慢性胃炎,并发展为更严重的疾病,包括消化性溃疡病和胃癌。幽门螺杆菌的长期携带是胃部疾病发病机制的最关键因素。细菌在胃黏膜中的持续存在取决于细菌因素以及宿主因素。本文对幽门螺杆菌感染初期的宿主和细菌成分进行了综述和讨论。阐述了细菌的黏附与适应,以解释幽门螺杆菌在胃黏膜中定植的持续性,其中包括细菌对宿主防御系统的逃避和基因组多样性。