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人胃上皮细胞膜神经节苷脂含量的改变可降低幽门螺杆菌的黏附。

Modification of Ganglioside Content of Human Gastric Epithelial Cell Membrane Decreases Helicobacter pylori Adhesion.

作者信息

Rivas-Serna Irma Magaly, Mazurak Vera C, Keelan Monika, Clandinin Michael Thomas

机构信息

*Department of Agricultural, Food and Nutritional Science†Department of Laboratory Medicine and Pathology‡Department of Medicine, University of Alberta, Edmonton, Alberta, Canada.

出版信息

J Pediatr Gastroenterol Nutr. 2017 Oct;65(4):456-461. doi: 10.1097/MPG.0000000000001612.

DOI:10.1097/MPG.0000000000001612
PMID:28945209
Abstract

BACKGROUND

In polarized cells, ganglioside location determines ganglioside function. Diet alters ganglioside content and composition in cell membranes. Ganglioside acts as a receptor for Helicobacter pylori. H pylori infects the stomach epithelium and may cause peptic ulcer disease and gastric cancer. The present study used purified gangliosides to modify the ganglioside composition of human gastric epithelial cells in vitro to reduce H pylori adhesion.

METHODS

A human gastric epithelial cell line (NCI-N87) was cultured with a ganglioside mix or with pure ganglioside (GM3 or GD3) at different concentrations (0-30 μg/mL) and ganglioside membrane content of gastric cells was determined after 48 hours. LC/triple quadrupole MS was used to analyse ganglioside concentration. H pylori was inoculated into the culture media of gastric cells previously treated with gangliosides GM3 or GD3 or a combination of GM3 and GD3.

RESULTS

GD3 and GM3 content increased in the plasma membrane in a dose-dependent manner. Gastric cells treated with GD3 showed more GM3 content than GD3 (P < 0.01). Ganglioside content was modified in the apical membrane, but GM3 and GD3 were also found in the basolateral membrane after treatments. Gastric cells treated with GM3, GD3 or the combination of GM3:GD3 decreased H pylori adhesion to gastric cells at all ganglioside concentrations tested by 80% compared with untreated gastric cells (P < 0.05).

CONCLUSIONS

These observations suggest that GD3 and GM3 present in the stomach lumen may be taken up into the apical gastric membrane and decrease H pylori adhesion to the epithelium.

摘要

背景

在极化细胞中,神经节苷脂的位置决定其功能。饮食会改变细胞膜中神经节苷脂的含量和组成。神经节苷脂可作为幽门螺杆菌的受体。幽门螺杆菌感染胃上皮,可能导致消化性溃疡疾病和胃癌。本研究使用纯化的神经节苷脂在体外改变人胃上皮细胞的神经节苷脂组成,以减少幽门螺杆菌的黏附。

方法

将人胃上皮细胞系(NCI-N87)与神经节苷脂混合物或不同浓度(0-30μg/mL)的纯神经节苷脂(GM3或GD3)一起培养,48小时后测定胃细胞的神经节苷脂膜含量。采用液相色谱/三重四极杆质谱分析神经节苷脂浓度。将幽门螺杆菌接种到先前用神经节苷脂GM3或GD3或GM3与GD3组合处理过的胃细胞培养基中。

结果

质膜中GD3和GM3含量呈剂量依赖性增加。用GD3处理的胃细胞显示GM3含量高于GD3(P<0.01)。顶膜中的神经节苷脂含量发生改变,但处理后在基底外侧膜中也发现了GM3和GD3。与未处理的胃细胞相比,用GM3、GD3或GM3:GD3组合处理的胃细胞在所有测试的神经节苷脂浓度下,幽门螺杆菌对胃细胞的黏附均降低了80%(P<0.05)。

结论

这些观察结果表明,胃腔中的GD3和GM3可能被吸收到胃顶膜中,并减少幽门螺杆菌对上皮的黏附。

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