幽门螺杆菌CagA及VacA致病机制的研究进展

涂宏飞; 费素娟

doi:10.3969/j.issn.1671-038X.2019.05.19

幽门螺杆菌CagA及VacA致病机制的研究进展

涂宏飞¹,
费素娟^2, ,

- 1. 徐州医科大学, 江苏徐州 22100;
- 2. 徐州医科大学附属医院消化内科, 江苏徐州 221002

详细信息

作者简介:
涂宏飞, 男, 在读硕士研究生, 研究方向:幽门螺杆菌致病机制

通讯作者: 费素娟, E-mail:xyfyfeisj99@163.com

中图分类号: R57

收稿日期: 2019-02-17

Corresponding author: , E-mail: xyfyfeisj99@163.com

Received Date: 17 February 2019

摘要

摘要: 幽门螺杆菌是世界上感染率最高的细菌之一^[1]。虽然在世界许多地区幽门螺杆菌的感染率较前有所下降,但世界上仍有近一半的人口受到幽门螺杆菌的影响^[2]。大多数感染幽门螺杆菌的人没有明显的临床症状,然而幽门螺杆菌是与消化系统疾病发展相关的一个重要因素。据统计,大约不到0.01%的幽门螺杆菌感染者发展为胃黏膜相关淋巴组织淋巴瘤（MALT）,0.1%～3%发展为胃癌,1%～10%发展为消化性溃疡,高达10%～15%将发展为幽门螺杆菌相关疾病^[3]
- 幽门螺杆菌 /
- CagA /
- VacA /
- 致病机制

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参考文献(33)

[1]	Shu L, Zheng PF, Zhang XY.Dietary patterns and Helicobacter pylori infection in a group of Chinese adults ages between 45 and 59 years old:An observational study[J].Medicine, 2019, 98 (2):e14113.
[2]	Mégraud F.Antibiotic Resistance Is the Key Element in Treatment of Helicobacter pylori Infection[J].Gastroenterology, 2018, 155 (5):1300-1302.
[3]	Nejati S, Karkhah A, Darvish H, et al.Influence of Helicobacter pylori virulence factors CagA and VacA on pathogenesis of gastrointestinal disorders[J].Microb Pathog, 2018, 117 (1):43-48.
[4]	Tran LS, Tran D, De Paoli A, et al.NOD1 is required for Helicobacter pylori induction of IL-33 responses in gastric epithelial cells[J].Cell Microbiol, 2018, 20 (5):e12826.
[5]	Tourani M, Habibzadeh M, Shokri-Shirvani J, et al.Association of Helicobacter pylori infection with Toll-like receptor-4 Thr399 Ile polymorphism increased the risk of peptic ulcer development in North of Iran[J].APMIS, 2018, 126 (1):76-84.
[6]	Khatoon J, Prasad KN, Rai RP, et al.Expression levels of A disintegrin and metalloproteases (ADAMs), and Th17-related cytokines and their association with Helicobacter pylori infection in patients with gastroduodenal diseases[J].Pathog Dis, 2018, 76 (8):224-228.
[7]	Kivrak Salim D, Sahin M, Köksoy S, et al.Local Immune Response in Helicobacter pylori Infection[J].Medicine, 2016, 95 (20):e3713.
[8]	Hong JB, Zuo W, Wang AJ.Helicobacter pylori Infection Synergistic with IL-1β Gene Polymorphisms Potentially Contributes to the Carcinogenesis of Gastric Cancer[J].Int J Med Sci, 2016, 13 (4):298-303.
[9]	Melchiades JL, Zabaglia LM, Sallas ML, et al.Polymorphisms and haplotypes of the interleukin 2 gene are associated with an increased risk of gastric cancer The possible involvement of Helicobacter pylori[J].Cytokine, 2017, 96:203-207.
[10]	Atrisco-Morales J, Martínez-Santos VI, Román-Román A, et al.vacA s1 m1 genotype and cagA EPIYA-ABC pattern are predominant among Helicobacter pylori strains isolated from Mexican patients with chronic gastritis[J].J Med Microbiol, 2018, 67 (3):314-324.
[11]	Safaralizadeh R, Dastmalchi N, Hosseinpourfeizi M, et al.Helicobacter pylori virulence factors in relation to gastrointestinal diseases in Iran[J].Microb Pathog, 2017, 105:211-217.
[12]	Bagheri N, Azadegan-Dehkordi F, Rafieian-Kopaei M, et al.Clinical relevance of Helicobacter pylori virulence factors in Iranian patients with gastrointestinal diseases[J].Microb Pathog, 2016, 100:154-162.
[13]	.Cherati M.R, Shokri-Shirvani J, Karkhah A, et al.Helicobacter pylori cagL amino acid polymorphism D58 E59 pave the way toward peptic ulcer disease while N58 E59 is associated with gastric cancer in north of Iran[J].Microb.Pathog, 2017, 107:413-418.
[14]	Steensma DP, Kyle RA.J Robin Warren:Helicobacter Pylori and Peptic Ulcer[J].Mayo Clin Proc, 2016, 91 (9):e129-130.
[15]	de Brito BB, da Silva FAF, de Melo FF.Role of polymorphisms in genes that encode cytokines and Helicobacter pylori virulence factors in gastric carcinogenesis[J].World J Clin Oncol, 2018, 9 (5):83-89.
[16]	Inagaki T, Nishiumi S, Ito Y, et al.Associations Between CagA, VacA, and the Clinical Outcomes of Helicobacter Pylori Infections in Okinawa, Japan[J].Kobe J Med Sci, 2017, 63 (2):E58-E67.
[17]	Phan TN, Santona A, Tran VH, et al.Genotyping of Helicobacter pylori shows high diversity of strains circulating in central Vietnam[J].Infect Genet Evol, 2017, 52:19-25.
[18]	Sokolova O.NF-κB Signaling in Gastric Cancer[J].Toxins, 2017, 9 (4):119-141.
[19]	Yang F, Xu Y, Liu C, et al.NF-κB/miR-223-3p/ARID1 A axis is involved in Helicobacter pylori CagA-induced gastric carcinogenesis and progression[J].Cell Death Dis, 2018, 9 (1):12-25.
[20]	魏茜, 余树林, 黄宜峰.胃癌组织中P53、IL-1β、NF-κB的表达及与幽门螺杆菌感染的相关性分析[J].中国中西医结合消化杂志, 2019, 27 (3):228-231.
[21]	Tran LS, Tran D, De Paoli A, et al.NOD1 is required for Helicobacter pylori induction of IL-33 responses in gastric epithelial cells[J].Cell Microbiol, 2018, 20 (5):e12826.
[22]	Tegtmeyer N, Wessler S, Necchi V, et al.Helicobacter pylori Employs a Unique Basolateral Type IV Secretion Mechanism for CagA Delivery[J].Cell Host Microbe, 2017, 22 (4):552-560.
[23]	Li N, Feng Y, Hu Y, et al.Helicobacter pylori CagA promotes epithelial mesenchymal transition in gastric carcinogenesis via triggering oncogenic YAP pathway[J].J Exp Clin Cancer Res, 2018, 37 (1):280-290.
[24]	Wang G, Romero-Gallo J, Benoit SL, et al.Hydrogen Metabolism in Helicobacter pylori Plays a Role in Gastric Carcinogenesis through Facilitating CagA Translocation[J].MBio, 2016, 7 (4):e01022-16.
[25]	McClain MS, Beckett AC.Helicobacter pylori Vacuolating Toxin and Gastric Cancer[J].Toxins, 2017, 9 (10):316-333.
[26]	Timothy L.Helicobacter pylori Diversity and Gastric Cancer Risk[J].MBio, 2016, 7 (1):1869-1884.
[27]	Bakhti SZ, Latifi-Navid S, Mohammadi S, et al.Relevance of Helicobacter pylori vacA 3'-end Region Polymorphism to Gastric Cancer[J].Helicobacter, 2016, 21 (4):305-316.
[28]	Kim IJ, Lee J, Oh SJ, et al.Helicobacter pylori Infection Modulates Host Cell Metabolism through VacA-Dependent Inhibition of mTORC1[J].Cell Host Microbe, 2018, 23 (5):583-593.
[29]	Chauhan N, Tay ACY, Marshall BJ.Helicobacter pylori VacA, a distinct toxin exerts diverse functionalities in numerous cells:An overview[J].Helicobacter, 2019, 24 (1):e12544.
[30]	Djekic A, Müller A.The immunomodulator VacA promotes immune tolerance and persistent Helicobacter pylori infection through its activities on T-cells and antigen-presenting cells[J].Toxins, 2016, 8 (6):E187-196.
[31]	Zhu P, Xue J, Zhang ZJ, et al.Helicobacter pylori VacA induces autophagic cell death in gastric epithelial cells via the endoplasmic reticulum stress pathway[J].Cell Death Dis, 2017, 8 (12):3207-3219.
[32]	Nejati S, Karkhah A, Darvish H, et al.Influence of Helicobacter pylori virulence factors CagA and VacA on pathogenesis of gastrointestinal disorders[J].Microb Pathog, 2018, 117:43-48.
[33]	Abdullah M, Greenfield LK, Bronte-Tinkew D, et al.VacA promotes CagA accumulation in gastric epithelial cells during Helicobacter pylori infection[J].Sci Rep, 2019, 9 (1):38-46.