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从一名胃黏膜巨大肥厚症患者分离出的幽门螺杆菌可增加胃成纤维细胞中肝细胞生长因子mRNA的表达:与从其他胃部疾病分离出的幽门螺杆菌的比较。

Helicobacter pylori isolated from a patient with Ménétrier's disease increases hepatocyte growth factor mRNA expression in gastric fibroblasts: comparison with Helicobacter pylori isolated from other gastric diseases.

作者信息

Ishikawa Takeshi, Ando Takashi, Obayashi Hiroshi, Nakabe Nami, Okita Mika, Isozaki Yutaka, Nagao Yasuyuki, Oyamada Hirokazu, Nakajima Yoshihiro, Kato Haruki, Kokura Satoshi, Naito Yuji, Yoshida Norimasa, Yoshikawa Toshikazu

机构信息

Department of Gastroenterology, Matsushita Memorial Hospital, 5-55 Sotojima-cho, Moriguchi City, Osaka 570-8540, Japan.

出版信息

Dig Dis Sci. 2008 Jul;53(7):1785-91. doi: 10.1007/s10620-007-0070-4. Epub 2007 Nov 8.

DOI:10.1007/s10620-007-0070-4
PMID:17990109
Abstract

Ménétrier's disease has been reported to be associated with Helicobacter pylori infection. The aim of this study was to investigate the genetic characteristics of various virulence factors and cytokine expression profiles in Helicobacter pylori isolated from patients with Ménétrier's disease. The genotyping of virulence factors was accomplished by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Induction of various cytokines in MKN45 cells or gastric fibroblasts by Helicobacter pylori stimulus was measured by real-time reverse transcription-PCR. We found that the Helicobacter pylori strain isolated from a patient with Ménétrier's disease was different from other strains in the MseI-RFLP pattern of the ureC gene. Helicobacter pylori isolated from a patient with Ménétrier's disease showed the highest hepatocyte growth factor (HGF) and TNF-alpha mRNA expressions from gastric fibroblasts, and the highest TNF-alpha expression from MKN45 cells. The results in this study suggest that the difference in cytokine production, depending on the difference in bacteria components, plays an important role in the development of Ménétrier's disease.

摘要

据报道,门脉性胃病与幽门螺杆菌感染有关。本研究的目的是调查从门脉性胃病患者分离出的幽门螺杆菌中各种毒力因子的遗传特征和细胞因子表达谱。毒力因子的基因分型通过聚合酶链反应-限制性片段长度多态性(PCR-RFLP)完成。通过实时逆转录PCR测定幽门螺杆菌刺激MKN45细胞或胃成纤维细胞中各种细胞因子的诱导情况。我们发现,从门脉性胃病患者分离出的幽门螺杆菌菌株在ureC基因的MseI-RFLP模式上与其他菌株不同。从门脉性胃病患者分离出的幽门螺杆菌在胃成纤维细胞中显示出最高的肝细胞生长因子(HGF)和TNF-α mRNA表达,在MKN45细胞中显示出最高的TNF-α表达。本研究结果表明,细胞因子产生的差异取决于细菌成分的差异,在门脉性胃病的发展中起重要作用。

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Dig Dis Sci. 2008 Jul;53(7):1785-91. doi: 10.1007/s10620-007-0070-4. Epub 2007 Nov 8.
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本文引用的文献

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Ménétrier's disease in a patient with Helicobacter pylori infection is linked to elevated glucagon-like peptide-2 activity.一名幽门螺杆菌感染患者所患的梅内特里耶病与胰高血糖素样肽-2活力升高有关。
Scand J Gastroenterol. 2005 Apr;40(4):477-81. doi: 10.1080/00365520510011461.
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Hepatocyte growth factor disrupts tight junctions in human breast cancer cells.肝细胞生长因子破坏人乳腺癌细胞中的紧密连接。
Cell Biol Int. 2004;28(5):361-71. doi: 10.1016/j.cellbi.2004.03.003.
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Mechanism of action of low recurrence of gastritis caused by Helicobacter pylori with the type II urease B gene.
幽门螺杆菌II型脲酶B基因导致胃炎低复发率的作用机制。
Helicobacter. 2004 Apr;9(2):173-80. doi: 10.1111/j.1083-4389.2004.00215.x.
4
Regulation of RPE intercellular junction integrity and function by hepatocyte growth factor.肝细胞生长因子对视网膜色素上皮细胞间连接完整性和功能的调节
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5
HGF regulates tight junctions in new nontumorigenic gastric epithelial cell line.肝细胞生长因子调节新的非致瘤性胃上皮细胞系中的紧密连接。
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6
Cytokine expression and production by purified Helicobacter pylori urease in human gastric epithelial cells.纯化的幽门螺杆菌尿素酶在人胃上皮细胞中的细胞因子表达与产生
Infect Immun. 2000 Feb;68(2):664-71. doi: 10.1128/IAI.68.2.664-671.2000.
7
Hepatocyte growth factor stimulates fetal gastric epithelial cell growth in vitro.肝细胞生长因子在体外刺激胎儿胃上皮细胞生长。
J Surg Res. 1998 Aug;78(2):161-8. doi: 10.1006/jsre.1997.5230.
8
Diversity of Helicobacter pylori vacA and cagA genes and relationship to VacA and CagA protein expression, cytotoxin production, and associated diseases.幽门螺杆菌vacA和cagA基因的多样性及其与VacA和CagA蛋白表达、细胞毒素产生及相关疾病的关系。
J Clin Microbiol. 1998 Apr;36(4):944-8. doi: 10.1128/JCM.36.4.944-948.1998.
9
Roles of hepatocyte growth factor and its receptor Met during gastric ulcer healing in rats.肝细胞生长因子及其受体Met在大鼠胃溃疡愈合过程中的作用。
Gastroenterology. 1997 Dec;113(6):1858-72. doi: 10.1016/s0016-5085(97)70005-2.
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