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Gastric epithelial cell death caused by Helicobacter suis and Helicobacter pylori γ-glutamyl transpeptidase is mainly glutathione degradation-dependent

Bram Flahou (UGent) , Freddy Haesebrouck (UGent) , Koen Chiers (UGent) , Kim Van Deun (UGent) , Lina De Smet (UGent) , Bart Devreese (UGent) , Isabel Vandenberghe (UGent) , Herman Favoreel (UGent) , Annemieke Smet (UGent) , Frank Pasmans (UGent) , et al.
(2011) CELLULAR MICROBIOLOGY. 13(12). p.1933-1955
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Abstract
Helicobacter (H.) suis is the most prevalent non-H. pylori Helicobacter species colonizing the stomach of humans suffering from gastric disease. In the present study, we aimed to unravel the mechanism used by H. suis to induce gastric epithelial cell damage. H. suis lysate induced mainly apoptotic death of human gastric epithelial cells. Inhibition of ?-glutamyl transpeptidase (GGT) activity present in H. suis lysate and incubation of AGS cells with purified native and recombinant H. suis GGT showed that this enzyme was partly responsible for the observed apoptosis. Supplementation of H. suis or H. pylori GGT-treated cells with glutathione strongly enhanced the harmful effect of both enzymes and resulted in the induction of oncosis/necrosis, demonstrating that H. suis and H. pylori GGT-mediated degradation of glutathione and the resulting formation of glutathione degradation products play a direct and active role in the induction of gastric epithelial cell death. This was preceded by an increase of extracellular H2O2 concentrations, generated in a cell-independent manner and causing lipid peroxidation. In conclusion, H. suis and H. pylori GGT-mediated generation of pro-oxidant glutathione degradation products brings on cell damage and causes apoptosis or necrosis, dependent on the amount of extracellular glutathione available as a GGT substrate.
Keywords
LIQUID-CHROMATOGRAPHY, APOPTOSIS, MUCOSAL LIPOPEROXIDATION, H2O2 PRODUCTION, GENOME SEQUENCE, MONGOLIAN GERBILS, HYDROGEN-PEROXIDE, REACTIVE OXYGEN, HEILMANNII, INFECTION

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Chicago
Flahou, Bram, Freddy Haesebrouck, Koen Chiers, Kim Van Deun, Lina De Smet, Bart Devreese, Isabel Vandenberghe, et al. 2011. “Gastric Epithelial Cell Death Caused by Helicobacter Suis and Helicobacter Pylori Γ-glutamyl Transpeptidase Is Mainly Glutathione Degradation-dependent.” Cellular Microbiology 13 (12): 1933–1955.
APA
Flahou, B., Haesebrouck, F., Chiers, K., Van Deun, K., De Smet, L., Devreese, B., Vandenberghe, I., et al. (2011). Gastric epithelial cell death caused by Helicobacter suis and Helicobacter pylori γ-glutamyl transpeptidase is mainly glutathione degradation-dependent. CELLULAR MICROBIOLOGY, 13(12), 1933–1955.
Vancouver
1.
Flahou B, Haesebrouck F, Chiers K, Van Deun K, De Smet L, Devreese B, et al. Gastric epithelial cell death caused by Helicobacter suis and Helicobacter pylori γ-glutamyl transpeptidase is mainly glutathione degradation-dependent. CELLULAR MICROBIOLOGY. 2011;13(12):1933–55.
MLA
Flahou, Bram, Freddy Haesebrouck, Koen Chiers, et al. “Gastric Epithelial Cell Death Caused by Helicobacter Suis and Helicobacter Pylori Γ-glutamyl Transpeptidase Is Mainly Glutathione Degradation-dependent.” CELLULAR MICROBIOLOGY 13.12 (2011): 1933–1955. Print.
@article{1982608,
  abstract     = {Helicobacter (H.) suis is the most prevalent non-H. pylori Helicobacter species colonizing the stomach of humans suffering from gastric disease. In the present study, we aimed to unravel the mechanism used by H. suis to induce gastric epithelial cell damage. H. suis lysate induced mainly apoptotic death of human gastric epithelial cells. Inhibition of ?-glutamyl transpeptidase (GGT) activity present in H. suis lysate and incubation of AGS cells with purified native and recombinant H. suis GGT showed that this enzyme was partly responsible for the observed apoptosis. Supplementation of H. suis or H. pylori GGT-treated cells with glutathione strongly enhanced the harmful effect of both enzymes and resulted in the induction of oncosis/necrosis, demonstrating that H. suis and H. pylori GGT-mediated degradation of glutathione and the resulting formation of glutathione degradation products play a direct and active role in the induction of gastric epithelial cell death. This was preceded by an increase of extracellular H2O2 concentrations, generated in a cell-independent manner and causing lipid peroxidation. In conclusion, H. suis and H. pylori GGT-mediated generation of pro-oxidant glutathione degradation products brings on cell damage and causes apoptosis or necrosis, dependent on the amount of extracellular glutathione available as a GGT substrate.},
  author       = {Flahou, Bram and Haesebrouck, Freddy and Chiers, Koen and Van Deun, Kim and De Smet, Lina and Devreese, Bart and Vandenberghe, Isabel and Favoreel, Herman and Smet, Annemieke and Pasmans, Frank and D'Herde, Katharina and Ducatelle, Richard},
  issn         = {1462-5814},
  journal      = {CELLULAR MICROBIOLOGY},
  keyword      = {LIQUID-CHROMATOGRAPHY,APOPTOSIS,MUCOSAL LIPOPEROXIDATION,H2O2 PRODUCTION,GENOME SEQUENCE,MONGOLIAN GERBILS,HYDROGEN-PEROXIDE,REACTIVE OXYGEN,HEILMANNII,INFECTION},
  language     = {eng},
  number       = {12},
  pages        = {1933--1955},
  title        = {Gastric epithelial cell death caused by Helicobacter suis and Helicobacter pylori \ensuremath{\gamma}-glutamyl transpeptidase is mainly glutathione degradation-dependent},
  url          = {http://dx.doi.org/10.1111/j.1462-5822.2011.01682.x},
  volume       = {13},
  year         = {2011},
}

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