Alterations in metabolic pathways in stomach of mice infected with Helicobacter pylori

被引:12
作者
Nishiumi, Shin [1 ]
Yoshida, Masaru [1 ,2 ,3 ]
Azuma, Takeshi [1 ]
机构
[1] Kobe Univ, Grad Sch Med, Dept Internal Med, Div Gastroenterol,Chuo Ku, 7-5-1 Kusunoki Cho, Kobe, Hyogo 6500017, Japan
[2] Kobe Univ, Grad Sch Med, Dept Internal Related, Div Metabol Res,Chuo Ku, Kobe, Hyogo 6500017, Japan
[3] AMED CREST, AMED, Chuo Ku, 7-5-1 Kusunoki Cho, Kobe, Hyogo 6500017, Japan
基金
日本学术振兴会;
关键词
Helicobacter pylori; Metabolome analysis; Liquid chromatography/mass spectrometry; Gas chromatography/mass spectrometry; Metabolite; INDOLEAMINE 2,3-DIOXYGENASE; GENE-EXPRESSION; GASTRIC-CANCER; PATHOGENESIS; INFLAMMATION; GLUTAMINE; GERBILS; CELLS;
D O I
10.1016/j.micpath.2017.05.027
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Numerous studies of Helicobacter pylori (H. pylori) have been performed, but few studies have evaluated the effects of H. pylori infections using metabolome analysis, which involves the comprehensive study of low molecular weight metabolites. In this study, the metabolites in the stomach tissue of mice that had been infected with H. pylori SS1 for 1, 3, or 6 months were analyzed, and then evaluations of various metabolic pathways were performed to gain novel understandings of H. pylori infections. As a result, it was found that the glycolytic pathway, the tricarboxylic acid cycle, and the choline pathway tended to be upregulated at 1 month after the H. pylori SS1 infection. The urea cycle tended to be downregulated at 6 months after the infection. High levels of some amino acids were observed in the stomach tissue of the H. pylon SS1-infected mice at 1 month after the infection, whereas low levels of many amino acids were detected at 3 and 6 months after the infection. These results suggest that H. pylori infection causes various metabolic alterations at lesional sites, and these alterations might be linked to the crosstalk between H. pylori and the host leading to transition of disease conditions. (C) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:78 / 85
页数:8
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