國家衛生研究院 NHRI:Item 3990099045/11389
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    题名: Helicobacter pylori cholesterol glucosylation modulates autophagy for increasing intracellular survival in macrophages
    作者: Lai, CH;Huang, JC;Cheng, HH;Wu, MC;Huang, MZ;Hsu, HY;Chen, YA;Hsu, CY;Pan, YJ;Chu, YT;Chen, TJ;Wu, YF;Sit, WY;Liu, JS;Chiu, YF;Wang, HJ;Wang, WC
    贡献者: Institute of Biotechnology and Pharmaceutical Research
    摘要: 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.
    日期: 2018-12
    關聯: Cellular Microbiology. 2018 Dec;20(12):Article number e12947.
    Link to: http://dx.doi.org/10.1111/cmi.12947
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1462-5814&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000450013100004
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85053454517
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