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Updated: Jun 28, 2026
Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
[Establishment of Mongolian gerbil model of long-term Helicobacter pylori infection]
Zhe Jin1, Fu-Lian Hu, Hong Wei
1Department of Digestive Medicine, Peking University First Hospital, Beijing 100034, China.
Objective:
To establish a model of long-term infection with Helicobacter pylori (Hp) in Mongolian gerbil (Meriones unguiculatus), and to investigate if Hp combined with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) has a synergistic effect to induce gastric mucosa injury. To investigate pathological changes of gastric mucosa during long-term Hp infection in Mongolian gerbil model.
Methods:
90 healthy male Mongolian gerbils were randomly divided into 4 groups: Hp group (n = 24) undergoing gastric perfusion of Hp suspension of the line NCTC11637 in brain-heart infusion (BHI) 10(8)-10(9) CFU/ml once a day for 10 days and then gastric perfusion of 1 ml normal saline (NS) once a day for 10 days since the 4th week after Hp perfusion, Hp + MNNG group (n = 24) undergoing gastric perfusion of Hp solution once a day for 10 days and then MNNG 1 ml (2 mg/ml) once a day for 10 days, MNNG group (n = 20) undergoing gastric perfusion of BHI once a day for 10 days and then gastric perfusion of MNNC once a day for 10 day since the 4th week after BHI perfusion, and control group (n = 22) undergoing gastric perfusion of BHI once a day for 10 days and then gastric perfusion of NS again once a day for 10 day since the 4th week after the BHI perfusion. 4 and 8 weeks 1 gerbil from the control group and 2 gerbils from the Hp and Hp + MNNG groups each were killed to observe the pathological changes and Hp colonization by liquid-based urease test and Warthin-Starry silver staining. 20 and 40 weeks after the Hp inoculation 10 gerbils from each group were killed to observe the pathology of the gastric mucosa.
Results:
(1) A Mongolian gerbil model of long-term Hp infection was successfully established. (2) Hp induced the process progressing from normal gastric mucosa --> chronic atrophic gastritis --> intestinal metaplasia --> dysplasia. Until 40 weeks after Hp infection, the gastric mucosa of the control group remained normal. Twenty weeks after Hp infection 3 gerbils in the Hp group and 1 gerbil in the Hp + MNNC group showed glandular atrophy and intestinal metaplasia respectively, and 40 weeks after infection, glandular atrophy, intestinal metaplasia, and dysplasia at different degrees in the gastric mucosa were seen in the three experimental groups. The pathological changes of the Hp + MNNG group were the most severe. The incidence rates of precancerous lesions of the Hp + MNNG group were significantly higher than those of the other groups, but no gastric carcinoma was found in the experimental animals.
Conclusion:
Hp colonizes stably in the glandular gastric mucosa of Mongolian gerbils. The histological changes after infection are similar to those of the Hp infected human being. Hp and MNNG both cause the injury of gastric mucosa. With synergistic effect, the two pathogenic agents attack the gastric mucosa, they cause more severe injury.
Insights
Helicobacter pylori (Hp) infection in Mongolian gerbils causes progressive gastric injury, leading to precancerous lesions. Combining Hp with MNNG significantly worsens these pathological changes, highlighting a synergistic effect on gastric mucosa damage.
Area of Science:
- Gastroenterology
- Pathology
- Microbiology
Background:
- Helicobacter pylori (Hp) infection is a major cause of gastritis and gastric cancer.
- Establishing reliable animal models is crucial for understanding Hp pathogenesis and developing interventions.
- The role of co-factors in Hp-induced gastric injury requires further investigation.
Purpose of the Study:
- To develop a long-term Mongolian gerbil model for Helicobacter pylori (Hp) infection.
- To assess the synergistic effect of Hp and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) on gastric mucosa injury.
- To characterize the pathological progression of gastric mucosa changes during chronic Hp infection.
Main Methods:
- A long-term Hp infection model was established in 90 male Mongolian gerbils.
- Animals were divided into Hp, Hp + MNNG, MNNG, and control groups.
- Gastric perfusion was used for Hp and/or MNNG administration, followed by serial sacrifice for pathological analysis and Hp colonization assessment.
Main Results:
- A successful long-term Hp infection model in Mongolian gerbils was established.
- Hp infection induced a progression from normal mucosa to chronic atrophic gastritis, intestinal metaplasia, and dysplasia over 40 weeks.
- The Hp + MNNG group exhibited the most severe pathological changes and a higher incidence of precancerous lesions compared to other groups.
Conclusions:
- Helicobacter pylori colonizes stably in the glandular gastric mucosa of Mongolian gerbils.
- The induced histological changes mimic those observed in Hp-infected humans.
- Hp and MNNG act synergistically to cause severe gastric mucosa injury, increasing the risk of precancerous lesions.
