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1
Helicobacter pylori infection: treatment.幽门螺杆菌感染:治疗
Curr Opin Gastroenterol. 2002 Jan;18(1):26-33. doi: 10.1097/00001574-200201000-00005.
2
Pathogenesis of Helicobacter pylori infection.
Curr Opin Gastroenterol. 2001 Jan;17(1):24-9. doi: 10.1097/00001574-200101000-00005.
3
Treatment of Helicobacter pylori infection.幽门螺杆菌感染的治疗。
Curr Opin Gastroenterol. 2000 Jan;16(1):32-9. doi: 10.1097/00001574-200001000-00006.
4
Helicobacter pylori VacA toxin promotes bacterial intracellular survival in gastric epithelial cells.幽门螺杆菌空泡毒素(VacA)促进细菌在胃上皮细胞内的存活。
Infect Immun. 2006 Dec;74(12):6599-614. doi: 10.1128/IAI.01085-06. Epub 2006 Sep 25.
5
Apoptosis in Helicobacter pylori gastritis is related to cagA status.幽门螺杆菌胃炎中的细胞凋亡与细胞毒素相关基因A(cagA)状态有关。
Helicobacter. 2006 Oct;11(5):469-76. doi: 10.1111/j.1523-5378.2006.00440.x.
6
Apoptosis and proliferation in gastric epithelium due to Helicobacter pylori: an immunohistochemical and ultrastructural study.幽门螺杆菌导致的胃上皮细胞凋亡与增殖:一项免疫组织化学和超微结构研究
Acta Gastroenterol Belg. 2006 Apr-Jun;69(2):191-6.
7
Epidemiology of Helicobacter pylori infection.幽门螺杆菌感染的流行病学
Helicobacter. 2006 Oct;11 Suppl 1:1-5. doi: 10.1111/j.1478-405X.2006.00429.x.
8
Helicobacter pylori lipopolysaccharide promotes a Th1 type immune response in immunized mice.幽门螺杆菌脂多糖在免疫小鼠中促进Th1型免疫反应。
Vaccine. 2006 Jun 5;24(23):4987-94. doi: 10.1016/j.vaccine.2006.03.043. Epub 2006 Mar 30.
9
Diverse phenotypes resulting from polyphosphate kinase gene (ppk1) inactivation in different strains of Helicobacter pylori.不同幽门螺杆菌菌株中多聚磷酸激酶基因(ppk1)失活导致的多样表型。
J Bacteriol. 2005 Nov;187(22):7687-95. doi: 10.1128/JB.187.22.7687-7695.2005.
10
Helicobacter pylori CagA induces a transition from polarized to invasive phenotypes in MDCK cells.幽门螺杆菌CagA诱导MDCK细胞从极化表型转变为侵袭性表型。
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小鼠适应性幽门螺杆菌在不同上皮细胞系中的黏附和侵袭

Adherence and invasion of mouse-adapted H pylori in different epithelial cell lines.

作者信息

Zhang Mao-Jun, Meng Fan-Liang, Ji Xiao-Yun, He Li-Hua, Zhang Jian-Zhong

机构信息

Department of Diagnostics, National Institute for Communicable Disease Control and Prevention, Chinese Center for Disease Control and Prevention, PO Box 5, Changping, Beijing 102206, China.

出版信息

World J Gastroenterol. 2007 Feb 14;13(6):845-50. doi: 10.3748/wjg.v13.i6.845.

DOI:10.3748/wjg.v13.i6.845
PMID:17352012
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4065918/
Abstract

AIM

To assess the adhesion and invasion abilities of different mouse adapted H pylori strains in different cell lines in vitro and investigate their effects on the virulence factors cagA and vacA.

METHODS

The adherence and invasion abilities of different H pylori strains in different epithelial cell lines were examined by the gentamycin protection assay. The null mutants of cagA and vacA were processed by direct PCR mutation method. The morphologic changes of different cell lines after H pylori attachment were examined by microscopy.

RESULTS

The densities of adherence to and invasion into cells in vitro were different from those in the mouse infection experiments. 88-3887 strain could invade and adhere to cells stronger than SS1 and X47. All tested strains had better adhering and invasive abilities in SCG-7901 cell. CagA and vacA minus mutants had the same invasion and adherent abilities as their wild types. In all strains and cell lines tested, only AGS cell had the significant hummingbird phenotype after inoculation with the 88-3887 wild-type.

CONCLUSION

Both the host cells and the bacteria play important parts in the invasion and adhesion abilities of H pylori. CagA and VacA are not related to the ability of invasion and adhesion of H pylori in different cell lines in vitro.

摘要

目的

评估不同小鼠适应株幽门螺杆菌在不同细胞系中的体外黏附与侵袭能力,并研究它们对毒力因子cagA和vacA的影响。

方法

采用庆大霉素保护试验检测不同幽门螺杆菌菌株在不同上皮细胞系中的黏附与侵袭能力。通过直接PCR突变法构建cagA和vacA的缺失突变体。用显微镜观察幽门螺杆菌黏附后不同细胞系的形态变化。

结果

体外细胞黏附与侵袭密度与小鼠感染实验不同。88 - 3887菌株对细胞的侵袭和黏附能力强于SS1和X47。所有测试菌株在SCG - 7901细胞中均具有较好的黏附与侵袭能力。CagA和vacA缺失突变体与其野生型具有相同的侵袭和黏附能力。在所有测试的菌株和细胞系中,仅AGS细胞接种88 - 3887野生型后出现明显的蜂鸟表型。

结论

宿主细胞和细菌在幽门螺杆菌的侵袭和黏附能力中均起重要作用。CagA和VacA与幽门螺杆菌在不同体外细胞系中的侵袭和黏附能力无关。