Gastric mucosal changes induced by long term infection with Helicobacter pylori in Mongolian gerbils: effects of bacteria eradication

Keto, Yoshihiro; Ebata, Misako; Okabe, Susumu

doi:10.1016/s0928-4257(01)00059-6

Cited by 33 publications

(23 citation statements)

References 15 publications

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“…In the gerbil stomach, H. pylori infection induces gastritis at 2 weeks, gastric ulcer at 6 months, and then progresses to induce gastric cancer at 15 months with highly stable prevalence (16,18,19,33). In the present study, we confirmed in 3-month-infected gerbils that severe edema, surface congestion and some bleeding spots were observed in most areas of the gastric corpus, except for the area just close to the greater curvature.…”

Section: Discussionsupporting

confidence: 77%

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New Frontiers in Gut Nutrient Sensor Research: Prophylactic Effect of Glutamine Against Helicobacter pylori–Induced Gastric Diseases in Mongolian Gerbils

et al. 2010

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Abstract. Ammonia is one of the important toxins produced by Helicobacter pylori (H. pylori), the major cause of peptic ulcer diseases. We examined whether glutamine or marzulene (a gastroprotective drug containing 1% sodium azulene and 99% glutamine) protects the gastric mucosa against H. pylori in vivo and investigated the mechanism underlying glutamine-induced mucosal protection against ammonia in gastric epithelial cells in vitro. Mongolian gerbils were fed for 3 months with a diet containing glutamine (2% -20%) or marzulene (20%) starting from 2 weeks or 2 years after H. pylori infection. Then, gastric mucosal changes were evaluated both macro-and microscopically. Cultured gastric epithelial cells were incubated in the presence of ammonia, with or without glutamine; and cell viability, ammonia accumulation, and chemokine production were determined. Gerbils exhibited edema, congestion, and erosion after 3-month infection; and after 2-year infection, they showed cancer-like changes in the gastric mucosa. Glutamine and marzulene significantly suppressed these pathological changes caused in the gastric mucosa by H. pylori infection. Ammonia was accumulated in the cells, resulting in an increase in chemokine production and a decrease in cell viability. These pathological responses were prevented by glutamine. In addition, glutamine decreased chemokine production and cell death through inhibition of cellular accumulation of ammonia, resulting in the prevention of H. pylori-induced gastric diseases in vivo. These results suggest that glutamine/marzulene would be useful for prophylactic treatment of H. pylori-induced gastric diseases in patients.

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Section: Discussionsupporting

confidence: 77%

“…In addition, intestinal metaplasia was also seen as judged from goblet cells with sialomucin. These pathological changes were similar to those observed in humans (4,34), indicating that the experimental system using gerbils is the best animal model for evaluation of H. pylori-induced gastric diseases (8,18,19,33).…”

Section: Discussionsupporting

confidence: 76%

New Frontiers in Gut Nutrient Sensor Research: Prophylactic Effect of Glutamine Against Helicobacter pylori–Induced Gastric Diseases in Mongolian Gerbils

et al. 2010

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“…26 With regard to gastric atrophy, beneficial effects from H. pylori eradication have been shown in experimental animal models, where gastric atrophy and intestinal metaplasia were reversed. [27][28][29] In human studies, gastric atrophy and metaplasia did not progress, [30][31][32][33] and sometimes even regressed 24,26,[34][35][36][37][38][39][40][41] in patients who had H. pylori eradicated. These data and the results of this study suggest that H. pylori eradication may help to reduce the gastric cancer risk in patients whose gastric atrophy has already expanded, although the impact of eradication is variable among patients according to the extent of gastric atrophy.…”

Section: Discussionmentioning

confidence: 99%

Baseline gastric mucosal atrophy is a risk factor associated with the development of gastric cancer after Helicobacter pylori eradication therapy in patients with peptic ulcer diseases

Mizuno²,

et al. 2007

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“…More interestingly, there is evidence that eradication of H. pylori in these animal models can reverse the abnormalities leading to cancer, thus proving the causal association between infection and cancer. [18][19][20] …”

Section: Epidemiological Evidencementioning

confidence: 99%

Helicobacter pylori infection and gastric cancer

Lochhead

El-Omar

2007

Best Practice & Research Clinical Gastroenterology

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Gastric mucosal changes induced by long term infection with Helicobacter pylori in Mongolian gerbils: effects of bacteria eradication

Cited by 33 publications

References 15 publications

New Frontiers in Gut Nutrient Sensor Research: Prophylactic Effect of Glutamine Against Helicobacter pylori–Induced Gastric Diseases in Mongolian Gerbils

New Frontiers in Gut Nutrient Sensor Research: Prophylactic Effect of Glutamine Against Helicobacter pylori–Induced Gastric Diseases in Mongolian Gerbils

Baseline gastric mucosal atrophy is a risk factor associated with the development of gastric cancer after Helicobacter pylori eradication therapy in patients with peptic ulcer diseases

Helicobacter pylori infection and gastric cancer

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