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Updated: Feb 10, 2026
Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Helicobacter pylori-infected C57BL/6 mice with different gastrointestinal microbiota have contrasting gastric
Zhongming Ge1, Alexander Sheh2, Yan Feng2
1Division of Comparative Medicine, the Massachusetts Institute of Technology, Cambridge, MA, 02139, USA. zge@mit.edu.
Abstract:
C57BL/6 (B6) mice from Taconic Sciences (Tac) and the Jackson Laboratory (Jax) were infected with H. pylori PMSS1 (Hp) for 16 week; there was no significant difference in the gastric histologic activity index between Hp infected Tac and Jax B6. However, the degree of gastric mucous metaplasia and Th1-associated IgG2c levels in response to Hp infection were increased in Tac mice over Jax mice, whereas the colonization levels of gastric Hp were higher by 8-fold in Jax B6 compared with Tac B6. Additionally, mRNA expression of gastric Il-1β, Il-17A and RegIIIγ were significantly lower in the infected Tac compared to the infected Jax mice. There were significant differences in the microbial community structures in stomach, colon, and feces between Jax and Tac B6 females. Differences in gastric microbial communities between Jax and Tac B6 females are predicted to affect the metagenome. Moreover, Hp infection perturbed the microbial community structures in the stomach, colon and feces of Jax mice, but only altered the colonic microbial composition of Tac mice. Our data indicate that the GI microbiome of Tac B6 mice is compositionally distinct from Jax B6 mice, which likely resulted in different pathological, immunological, and microbial responses to Hp infection.
Insights
Differences in mouse gut microbiomes between suppliers impact Helicobacter pylori (Hp) infection outcomes. Taconic mice showed higher Hp-induced metaplasia and IgG2c, while Jax mice had greater Hp colonization and altered gut microbial communities.
Area of Science:
- Microbiology
- Immunology
- Genomics
Background:
- The gut microbiome plays a crucial role in host-pathogen interactions.
- Strain-specific differences in mouse models can influence experimental outcomes.
- Helicobacter pylori infection is a significant global health concern.
Purpose of the Study:
- To investigate the impact of distinct C57BL/6 mouse sources on H. pylori infection.
- To compare pathological, immunological, and microbial responses to H. pylori between mouse suppliers.
- To elucidate the role of the gut microbiome in modulating H. pylori pathogenesis.
Main Methods:
- Infection of C57BL/6 mice from Taconic and Jackson Laboratory with H. pylori PMSS1 for 16 weeks.
- Assessment of gastric histology, serum IgG2c levels, and H. pylori colonization.
- Analysis of gastric mRNA expression (Il-1β, Il-17A, RegIIIγ) and microbial community structures (stomach, colon, feces) using sequencing.
Main Results:
- No significant difference in gastric histologic activity index between groups.
- Taconic mice exhibited increased gastric mucous metaplasia and Th1-associated IgG2c levels.
- Jax mice showed 8-fold higher gastric H. pylori colonization and distinct alterations in gut microbial communities post-infection.
- Taconic mice had lower gastric Il-1β, Il-17A, and RegIIIγ mRNA expression compared to Jax mice.
- Significant differences in gut microbial community structures were observed between Taconic and Jax mice, irrespective of H. pylori infection.
Conclusions:
- The compositional distinctiveness of the gut microbiome in Taconic versus Jackson Laboratory C57BL/6 mice significantly influences pathological, immunological, and microbial responses to H. pylori infection.
- Host microbiome variation is a critical factor to consider in H. pylori research and other host-pathogen studies.
- Understanding these microbiome-driven differences can lead to more refined experimental designs and therapeutic strategies for H. pylori-associated diseases.
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