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Updated: Dec 31, 2025
Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Improved method for inducing chronic atrophic gastritis in mice
Xian Wei1, Xue-Ping Feng1, Lu-Yao Wang1
1Breeding Base of Microbial Infection Key Laboratory in the West Guangxi, Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China.
Background:
Chronic atrophic gastritis (CAG) is a common disease of the digestive system with pathological characteristics of a decreasing number, or disappearance, of inherent glands of the gastric mucosa. CAG has been defined as a precancerous condition of gastric cancer. Intestinal metaplasia or intraepithelial neoplasia accompanying atrophied glands of the stomach is regarded as one of the most important precancerous lesions of gastric cancer. As a common malignant tumour, gastric cancer remains without a satisfactory therapy and its pathogenesis remains unclear, seriously threatening human life. Therefore, some scholars have proposed to prevent the incidence of gastric cancer by avoiding precancerous lesions. If CAG can be reversed, the incidence of gastric cancer can be substantially reduced. To reverse and prevent CAG and study its pathogenesis and therapy, it is necessary to develop an ideal, safe, stable, animal model.
Aim:
To study a rapid, stable, and safe method of establishing a mouse model of human CAG.
Methods:
Six-week-old Kunming mice were divided into a phosphate buffered solution control group, a Helicobacter pylori (H. pylori) group, an N-methyl-N'-nitroguanidine (MNNG) group, an ammonia water group, and a group combining H. pylori, MNNG, and ammonia water (hereinafter referred to as the combined group). The mice were administrated with drinking water containing ammonia or infected with H. pylori through gavage. At the 30th, 60th, 90th, and 120th day after the last H. pylori infection, mice were selected randomly to collect their gastric mucosa for hematoxylin eosin staining, terminal nick-end labelling staining detection, and immunohistochemical staining for Bax and Bcl-2. In addition, H. pylori was isolated, cultured, and identified, and its extent of colonisation calculated. Blood was collected to detect inflammatory factors interleukin (IL)-1β, IL-8, and tumor necrosis factor (TNF)-α and immune function markers CD4 and CD8 to confirm successful establishment of the CAG model.
Results:
The combined group showed slight CAG at the 90th day and moderate CAG at the 120th day, while other groups did not show CAG at that time.
Conclusion:
The combination of H. pylori, MNNG, and ammonia is an effective method of developing a mouse model of human CAG.
