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Your search keyword '"Huang, Mei-Zi"' showing total 18 results
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18 results on '"Huang, Mei-Zi"'

10. Helicobacter pyloricholesterol glucosylation modulates autophagy for increasing intracellular survival in macrophages

Author

Lai, Chih-Ho, primary, Huang, Ju-Chun, additional, Cheng, Hsin-Hung, additional, Wu, Meng-Chen, additional, Huang, Mei-Zi, additional, Hsu, Hui-Ying, additional, Chen, Yu-An, additional, Hsu, Chung-Yao, additional, Pan, Yi-Jiun, additional, Chu, Yen-Ting, additional, Chen, Tsan-Jan, additional, Wu, Yu-Fang, additional, Sit, Wei Yang, additional, Liu, Jai-Shin, additional, Chiu, Ya-Fang, additional, Wang, Hung-Jung, additional, and Wang, Wen-Ching, additional

Published
2018
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11. Cytolethal Distending Toxin Enhances Radiosensitivity in Prostate Cancer Cells by Regulating Autophagy

Author

Lin, Hwai-Jeng, primary, Liu, Hsin-Ho, additional, Lin, Chia-Der, additional, Kao, Min-Chuan, additional, Chen, Yu-An, additional, Chiang-Ni, Chuan, additional, Jiang, Zhi-Pei, additional, Huang, Mei-Zi, additional, Lin, Chun-Jung, additional, Lo, U-Ging, additional, Lin, Li-Chiung, additional, Lai, Cheng-Kuo, additional, Lin, Ho, additional, Hsieh, Jer-Tsong, additional, Chiu, Cheng-Hsun, additional, and Lai, Chih-Ho, additional

Published
2017
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14. Helicobacter pylori Activates HMGB1 Expression and Recruits RAGE into Lipid Rafts to Promote Inflammation in Gastric Epithelial Cells

Author

Lin, Hwai-Jeng, primary, Hsu, Fang-Yu, additional, Chen, Wei-Wei, additional, Lee, Che-Hsin, additional, Lin, Ying-Ju, additional, Chen, Yi-Ywan M., additional, Chen, Chih-Jung, additional, Huang, Mei-Zi, additional, Kao, Min-Chuan, additional, Chen, Yu-An, additional, Lai, Hsin-Chih, additional, and Lai, Chih-Ho, additional

Published
2016
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15. Molecular Mechanisms and Potential Clinical Applications of Campylobacter jejuni Cytolethal Distending Toxin

Author

Lai, Cheng-Kuo, primary, Chen, Yu-An, additional, Lin, Chun-Jung, additional, Lin, Hwai-Jeng, additional, Kao, Min-Chuan, additional, Huang, Mei-Zi, additional, Lin, Yu-Hsin, additional, Chiang-Ni, Chuan, additional, Chen, Chih-Jung, additional, Lo, U-Ging, additional, Lin, Li-Chiung, additional, Lin, Ho, additional, Hsieh, Jer-Tsong, additional, and Lai, Chih-Ho, additional

Published
2016
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17. Helicobacter pylori Induces IL-33 Production and Recruits ST-2 to Lipid Rafts to Exacerbate Inflammation.

Author

Kuo, Chia-Jung, Chen, Chun-Ya, Lo, Horng-Ren, Feng, Chun-Lung, Wu, Hui-Yu, Huang, Mei-Zi, Liao, Tung-Nan, Chen, Yu-An, and Lai, Chih-Ho

Subjects
LIPID rafts, HELICOBACTER pylori, INTERLEUKIN-33, GASTRITIS, MEMBRANE lipids, EPITHELIAL cells
Abstract

Helicobacter pylori colonizes human gastric epithelial cells and contributes to the development of several gastrointestinal disorders. Interleukin (IL)-33 is involved in various immune responses, with reported proinflammatory and anti-inflammatory effects, which may be associated with colitis and colitis-associated cancer. IL-33 induces the inflammatory cascade through its receptor, suppression of tumorigenicity-2 (ST-2). Binding of IL-33 to membrane-bound ST-2 (mST-2) recruits the IL-1 receptor accessory protein (IL-1RAcP) and activates intracellular signaling pathways. However, whether IL-33/ST-2 is triggered by H. pylori infection and whether this interaction occurs in lipid rafts remain unclear. Our study showed that both IL-33 and ST-2 expression levels were significantly elevated in H. pylori-infected cells. Confocal microscopy showed that ST-2 mobilized into the membrane lipid rafts during infection. Depletion of membrane cholesterol dampened H. pylori-induced IL-33 and IL-8 production. Furthermore, in vivo studies revealed IL-33/ST-2 upregulation, and severe leukocyte infiltration was observed in gastric tissues infected with H. pylori. Together, these results demonstrate that ST-2 recruitment into the lipid rafts serves as a platform for IL-33-dependent H. pylori infection, which aggravates inflammation in the stomach. [ABSTRACT FROM AUTHOR]

Published
2019
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18. Helicobacter pylori cholesterol glucosylation modulates autophagy for increasing intracellular survival in macrophages.

Author

Lai, Chih‐Ho, Huang, Ju‐Chun, Cheng, Hsin‐Hung, Wu, Meng‐Chen, Huang, Mei‐Zi, Hsu, Hui‐Ying, Chen, Yu‐An, Hsu, Chung‐Yao, Pan, Yi‐Jiun, Chu, Yen‐Ting, Chen, Tsan‐Jan, Wu, Yu‐Fang, Sit, Wei Yang, Liu, Jai‐Shin, Chiu, Ya‐Fang, Wang, Hung‐Jung, and Wang, Wen‐Ching

Subjects
HELICOBACTER pylori, CHOLESTEROL, AUTOPHAGY, BIOSYNTHESIS, POLYSACCHARIDES
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. [ABSTRACT FROM AUTHOR]

Published
2018
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