We have located links that may give you full text access.
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Gastric ulcer, atrophic gastritis, and intestinal metaplasia caused by Helicobacter pylori infection in Mongolian gerbils.
BACKGROUND: Helicobacter pylori infection is associated with gastroduodenal disease in humans. In this study we aimed to show this relationship directly in Mongolian gerbils.
METHODS: The animals were challenged orally with H. pylori and killed 1, 2, 3, and 6 months after inoculation for histologic and anti-H. pylori antibody titer examination.
RESULTS: The spiral bacteria were observed in the mucus and gastric pits of all infected animals. A severe infiltration of the lamina propria by polymorphonuclear and mononuclear cells was seen 1 month after H. pylori inoculation. The submucosa was infiltrated by mainly mononuclear cells with formation of lymphoid follicles. Erosion of the gastric mucosa appeared soon after inoculation, whereas gastric ulcers, gastritis cystica profunda, and atrophy with goblet cell metaplasia occurred between 3 and 6 months after inoculation. In the duodenal mucosa a mild inflammatory cell infiltration with ballooning and diminished number of duodenal glands was seen. The IgG anti-H. pylori antibody titer increased gradually after 2 months of inoculation.
CONCLUSIONS: Since the gastritis, gastric ulcers, atrophic gastritis, and intestinal metaplasia that developed in Mongolian gerbils were similar to those observed in humans, this model may be useful to study the therapy of gastric ulcer and, with a longer observation period, to confirm a possible relationship between H. pylori and malignancy.
METHODS: The animals were challenged orally with H. pylori and killed 1, 2, 3, and 6 months after inoculation for histologic and anti-H. pylori antibody titer examination.
RESULTS: The spiral bacteria were observed in the mucus and gastric pits of all infected animals. A severe infiltration of the lamina propria by polymorphonuclear and mononuclear cells was seen 1 month after H. pylori inoculation. The submucosa was infiltrated by mainly mononuclear cells with formation of lymphoid follicles. Erosion of the gastric mucosa appeared soon after inoculation, whereas gastric ulcers, gastritis cystica profunda, and atrophy with goblet cell metaplasia occurred between 3 and 6 months after inoculation. In the duodenal mucosa a mild inflammatory cell infiltration with ballooning and diminished number of duodenal glands was seen. The IgG anti-H. pylori antibody titer increased gradually after 2 months of inoculation.
CONCLUSIONS: Since the gastritis, gastric ulcers, atrophic gastritis, and intestinal metaplasia that developed in Mongolian gerbils were similar to those observed in humans, this model may be useful to study the therapy of gastric ulcer and, with a longer observation period, to confirm a possible relationship between H. pylori and malignancy.
Full text links
Trending Papers
A Personalized Approach to the Management of Congestion in Acute Heart Failure.Heart International 2023
Potential Mechanisms of the Protective Effects of the Cardiometabolic Drugs Type-2 Sodium-Glucose Transporter Inhibitors and Glucagon-like Peptide-1 Receptor Agonists in Heart Failure.International Journal of Molecular Sciences 2024 Februrary 21
The Effect of Albumin Administration in Critically Ill Patients: A Retrospective Single-Center Analysis.Critical Care Medicine 2024 Februrary 8
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app