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- W2889203991 endingPage "e12947" @default.
- W2889203991 startingPage "e12947" @default.
- W2889203991 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." @default.
- W2889203991 created "2018-09-07" @default.
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- W2889203991 date "2018-09-17" @default.
- W2889203991 modified "2023-10-16" @default.
- W2889203991 title "<i>Helicobacter pylori</i>cholesterol glucosylation modulates autophagy for increasing intracellular survival in macrophages" @default.
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- W2889203991 doi "https://doi.org/10.1111/cmi.12947" @default.
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