H pylori bacteria
Helicobacter pylori bacteria damage to the mucosa of the stomach can start the development of chronic gastritis, peptic ulcers, and even gastric cancer.
Mechanisms include the directly toxic effects of Helicobacter pylori virulence, increased inflammation, oxidative stress, damage to DNA, and cellular death. One pathway that creates these damage signals is the glycosylation of TLR-4 (toll-like receptor 4).
Green tea has shown protective effects against gastritis caused by H. pylori.
EGCG from green tea blocks damage
A gastric mucosal cell study tested EGCG from green tea on the TLR-4 pathway.
Researchers found when they infected cells with Helicobacter pylori bacteria, damage included cellular death stimulated by the TLR-4 glycosylation pathway.
However, when the cells were pretreated with EGCG, that pathway was completely blocked, and other damaging pathways including extracellular signal response kinase and nuclear factor-kappaB were inactivated.
EGCG also reduced the production of inflammatory acids (Lee, Protective mechanism of epigallocatechin-3-gallate against Helicobacter pylori-induced gastric epithelial cytotoxicity via the blockage of TLR-4 signaling, Helicobacter, December 2004).
H. pylori is the most widespread infection among humans, affecting about half the world’s population.
This bacteria resides in the stomach creating chronic inflammation which can develop into chronic gastritis, and is associated with an increased lifetime risk of stomach cancer.
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This page last updated by Sharon Jones on January 4, 2013
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