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Glutamate supplementation prevents Helicobacter pylori‐induced gastric mucosal damages in gerbils
Author(s) -
Nakamura Eiji,
Amagase Kikuko,
Hasumura Mai,
Gabriel Ana San,
Uneyama Hisayuki,
Torii Kunio,
Takeuchi Koji
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1138.13
Subject(s) - helicobacter pylori , glutamate receptor , gastric mucosa , stomach , gastritis , helicobacter , urease , medicine , gastroenterology , biology , enzyme , biochemistry , receptor
Backgrounds & Aims: Chronic Helicobacter pylori (HP) infection induces gastric diseases such as gastritis, gastric ulcers and gastric cancers. The importance of urease‐derived ammonia in the pathogenesis of HP‐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 (Am J Physiol 2002). However, whether glutamate protects in vivo gastric mucosa against HP is still unknown. Thus, we examined the effect of glutamate supplementation on HP i ‐induced gastric mucosal damage using gerbil model. Materials & Methods: The diets with or without glutamate supplementation were fed to HP i ‐infected Mongolian gerbils for 3 months, then the gastric mucosa were used for the macroscopic, histochemical analyses. The number of viable HP in the stomach was also determined. Results & Discussion: Glutamate supplementation significantly suppressed HP‐induced gastric mucosal damage and inflammatory cell infiltration. Interestingly, the number of viable HP in the stomach was unchanged between the diet with and without glutamate. Conclusion: Glutamate supplementation protects HP‐induced gastric mucosal damage without affecting HP itself, suggesting the stimulatory role of glutamate on gastric defensive factors.