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Updated: Aug 22, 2026
Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Experimental Helicobacter felis infection in transgenic mice expressing human group IIA phospholipase A2
Heikki T Huhtinen1, Juha M Grönroos, Jaakko Uksila
1Department of Surgery, University of Turku and Turku University Central Hospital, Turku, Finland. heikki.huhtinen@fimnet.fi
Background:
Both various virulence factors of Helicobacter pylori and host factors influence the clinical outcome of H. pylori infection. In animal experiments with Helicobacter felis, large variations in the severity of disease have been observed between different mouse strains infected with a single isolate of H. felis. C57BL/6 J mouse strain that lacks the expression of group IIA phospholipase A2 has been shown to develop more severe gastric inflammation than other mouse strains. Thus, group IIA phospholipase A2 has been suggested to play a role in regulating inflammation in gastric mucosa. The aim of this study was to examine the possible role of group IIA phospholipase A2 in experimental Helicobacter infection.
Materials And Methods:
Transgenic mice expressing human group IIA phospholipase A2 and their group IIA phospholipase A2 deficient nontransgenic C57BL/6 J littermates were infected with H. felis. The mice were killed 3, 8, and 19 weeks after inoculation of bacteria to determine the histopathological changes in gastric mucosa.
Results:
The infected mice developed chronic inflammation in gastric mucosa. We found no differences in the colonization of bacteria between transgenic and nontransgenic mice. At 3 and 8 weeks, no difference was found in the severity of inflammation between the two groups. Nineteen weeks after the administration of bacteria the inflammation was more marked in nontransgenic than transgenic mice. Group IIA phospholipase A2 was expressed by in situ hybridization in the neck cells of the glandular stomach in transgenic mice.
Conclusions:
The results of the present study suggest that the endogenous expression of group IIA phospholipase A2 diminishes chronic inflammation in gastric mucosa in experimental H. felis infection in mice.
Insights
Group IIA phospholipase A2 expression reduces chronic gastric inflammation in mice infected with Helicobacter felis. This suggests a protective role for endogenous group IIA phospholipase A2 in regulating inflammation during H. felis infection.
Area of Science:
- Gastroenterology
- Immunology
- Microbiology
Background:
- Host factors significantly influence Helicobacter pylori infection outcomes.
- C57BL/6 J mice lacking group IIA phospholipase A2 show severe gastric inflammation.
- Group IIA phospholipase A2 is implicated in regulating gastric mucosal inflammation.
Purpose of the Study:
- To investigate the role of group IIA phospholipase A2 in experimental Helicobacter infection.
- To assess the impact of group IIA phospholipase A2 on gastric inflammation severity.
Main Methods:
- Transgenic mice expressing human group IIA phospholipase A2 and deficient littermates were infected with Helicobacter felis.
- Histopathological analysis of gastric mucosa was performed at 3, 8, and 19 weeks post-infection.
Main Results:
- All infected mice developed chronic gastric inflammation.
- No differences in bacterial colonization were observed between groups.
- Nontransgenic mice exhibited more severe inflammation than transgenic mice at 19 weeks post-infection.
- Group IIA phospholipase A2 expression was confirmed in the glandular stomach neck cells of transgenic mice.
Conclusions:
- Endogenous group IIA phospholipase A2 expression mitigates chronic gastric inflammation in experimental H. felis infection.
- Group IIA phospholipase A2 plays a protective role in the gastric mucosa during H. felis infection.
