Helicobacter pylori cholesterol glucosylation modulates autophagy for increasing intracellular survival in macrophages
Autor: | Ya-Fang Chiu, Hui-Ying Hsu, Yen-Ting Chu, Hsin-Hung Cheng, Jai-Shin Liu, Wen-Ching Wang, Yi-Jiun Pan, Hung-Jung Wang, Chung-Yao Hsu, Wei Yang Sit, Yu-Fang Wu, Mei-Zi Huang, Meng-Chen Wu, Yu-An Chen, Chih Ho Lai, Tsan-Jan Chen, Ju-Chun Huang |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Autophagosome maturation Immunology Mutant Biology Microbiology Helicobacter Infections 03 medical and health sciences chemistry.chemical_compound Gene Knockout Techniques Mice Membrane Microdomains Bacterial Proteins Virology Autophagy Macrophage Animals Lipid raft Gene knockdown Helicobacter pylori Cholesterol Macrophages Autophagosomes Cell biology 030104 developmental biology chemistry Glucosyltransferases Host-Pathogen Interactions Lysosomes Intracellular Autophagy-Related Protein 12 |
Zdroj: | Cellular microbiology. 20(12) |
ISSN: | 1462-5822 |
Popis: | 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. |
Databáze: | OpenAIRE |
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