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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/111898

    Title: Helicobacter pylori cholesterol glucosylation modulates autophagy for increasing intracellular survival in macrophages
    Authors: 賴志河;Lai, Chih-Ho;Huan, Ju-Chun;Huang, Ju-Chun;Ch, Hsin-Hung;Cheng, Hsin-Hung;Wu, Meng-Chen;Wu, Meng-Chen;Huang, Mei-Zi;Huang, Mei-Zi;Hsu, Hui-Ying;Hsu, Hui-Ying
    Contributors: 健康產業管理學系
    Date: 2018-11
    Issue Date: 2019-09-02 14:15:27 (UTC+8)
    Abstract: Cholesterol‐α‐glucosyltransferase (CGT) encoded by the type 1 capsular polysaccharide biosynthesis protein J (capJ) gene of Helicobacter pylori converts cellular cholesterol into cholesteryl glucosides. H. pylori infection induces autophagy that may increase bacterial survival in epithelial cells. However, the role of H. pylori CGT that exploits lipid rafts in interfering with autophagy for bacterial survival in macrophages has not been investigated. Here, we show that wild‐type H. pylori carrying CGT modulates cholesterol to trigger autophagy and restrain autophagosome fusion with lysosomes, permitting a significantly higher bacterial burden in macrophages than that in a capJ‐knockout (∆CapJ) mutant. Knockdown of autophagy‐related protein 12 impairs autophagosome maturation and decreases the survival of internalised H. pylori in macrophages. These results demonstrate that CGT plays a crucial role in the manipulation of the autophagy process to impair macrophage clearance of H. pylori.
    Appears in Collections:[健康產業管理學系] 期刊論文

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