Topic Highlight
Copyright ©2014 Baishideng Publishing Group Co.
World J Gastroenterol. Jan 21, 2014; 20(3): 630-638
Published online Jan 21, 2014. doi: 10.3748/wjg.v20.i3.630
Table 1 Reported Helicobacter pylori gamma-glutamyl transpeptidase effects
Involved in H. pylori colonization and persistence in the gastric mucosa[5,6]
Hydrolysis of extracellular glutamine and glutathione to generate glutamate that is transported into the H. pylori cell[8]
Highly active periplasmic deamidase involved in ammonia production[8,20]
Significantly higher GGT activity in strains obtained from patients with peptic ulcer disease[21]
Gastric epithelial cell death - Mitochondria-mediated apoptosis in gastric epithelial cells[7,16,24]
Cell-cycle arrest of gastric epithelial cells[24]
Glutathione degradation-dependent gastric epithelial cell death[8,27]
H2O2 generation, nuclear factor-κB activation and interleukin-8 production in gastric epithelial cells[21,27]
Induction of EGF-related growth factors and COX-2 in gastric epithelial cells[15]
Induction of apoptosis and inflammation in human biliary cells[25]
Degradation of the apoptosis-inhibiting protein survivin in gastric epithelial cells[30]
Inhibition of T cell proliferation and induction of G1 cell cycle arrest[9-11]
Induction of microRNA-155 in human T cells[38]
Gastric persistence and immune tolerance[12]