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Link Ammonia and Epithelial Cell Death Mechanisms in Helicobacter pylori Infection

Link Ammonia and Epithelial Cell Death Mechanisms in Helicobacter pylori Infection

Ji Hye Seo, James G. Fox, Richard M. Peek Jr, Susan J. Hagen

141:6, September 16, 2011

Link Ammonia and Epithelial Cell Death Mechanisms in Helicobacter pylori Infection

Background & Aims
Helicobacter pylori infection is a risk factor for gastric cancer. Ammonia/ammonium (A/A) is a cytotoxin generated by H pylori that kills gastric epithelial cells. We investigated whether A/A cytotoxicity occurs by activating N-methyl d-aspartate (NMDA) channels, which results in Ca2+ permeation and epithelial cell death.

Gastric epithelial cells were cultured to confluence and then incubated with A/A and NMDA channel or cell signaling antagonists. Cells were incubated with wild-type H pylori or mutant strains that do not produce A/A. Changes in intracellular Ca2+ were examined in living cells by confocal microscopy. Biochemical and histochemical techniques were used to examine the relationship between A/A-induced cell death and intracellular levels of Ca2+.

A/A increased Ca2+ permeation in gastric epithelial cells; the increase was blocked by NMDA receptor and cell signaling antagonists. Wild-type, but not mutant H pylori, also caused extensive Ca2+ permeation of gastric epithelial cells, which was blocked when NMDA-receptor expression was repressed. Ca2+ that entered cells was initially cytoplasmic and activated proteases. Later, the Ca2+ was sequestered to cytoplasmic vacuoles that are dilatations of the endoplasmic reticulum. Inositol-3-phosphate–dependent release of Ca2+ from the endoplasmic reticulum and protease activity damaged mitochondria, reduced levels of adenosine triphosphate, and transcriptionally up-regulated cell death effectors. Expression of the NMDA receptor was altered in stomachs of mice infected with H pylori.

A/A affects gastric epithelial cell viability by allowing excessive Ca2+ permeation through NMDA channels. NMDA channels might thereby regulate cell survival and death pathways during development of gastric cancers associated with H pylori infection.

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Prepared by: Dr. Houssam Al-Nahhas

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