Glutamate supplementation protects gerbil gastric mucosa against Helicobacter pylori

Backgrounds & Aims: The importance of urease-derived ammonia in the pathogenesis of Helicobacter pylori (H. pylori)-induced gastric diseases is known by the fact that Helicobacter felis (expresses urease but not vac A or cag PAI-related gene products) induces gastritis and gastric cancer in animal models. Glutamate is previously reported to protect cultured gastric epithelial cells against ammonia (Nakamura & Hagen, Am J Physiol 283: G1264, 2002). However, whether glutamate protects in vivo gastric mucosa against H. pylori is still unknown. Thus, we examined the effect of glutamate supplementation on H. pylori-induced gastric mucosal damage using gerbil model.Materials & Methods: The diets with or without glutamate supplementation were fed to H. pylori-infected Mongolian gerbils for 3 months, then the gastric mucosa were used for the macroscopic, histochemical analyses. The number of viable H. pylori in the stomach was also determined. Results & Discussion: Glutamate supplementation significantly suppressed H. pylori-induced gastric mucosal damage and inflammatory cell infiltration. Interestingly, the number of viable H. pylori in the stomach was unchanged between the diet with and without glutamate.Conclusion: Glutamate supplementation protects H. pylori-induced gastric mucosal damage without affecting H. pylori itself, suggesting the stimulatory role of glutamate on gastric defensive factors. [J Physiol Sci. 2008;58 Suppl:S214]