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Updated: Dec 23, 2025
Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Effects of Colonization of Gnotobiotic Swiss Webster Mice with Helicobacter bilis
Mark T Whary1, Chuanwu Wang2, Catherine F Ruff2
1Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, Massachusetts;,
Abstract:
Helicobacter bilis (Hb) causes hepatitis in some strains of inbred mice. The current study confirmed that Hb directly causes portal hepatitis in outbred gnotobiotic Swiss Webster (SW) mice, as we previously reported for conventional SW mice. Hbmonoassociated SW mice also developed mild enterocolitis, expanded gut-associated lymphoid tissue (GALT), and tertiary lymphoid tissue in the lower bowel. At 1 and 10 mo after infection, Hb-induced GALT hyperplasia exhibited well-organized, ectopic germinal centers with increased mononuclear cell apoptosis, MHC class II antigen presentation, and pronounced endothelial venule formation, consistent with features of tertiary lymphoid tissue. In the lower bowel, Hb induced mainly B220+ cells as well as CD4+ IL17+, CD4+ IFNγ+, and CD4+ FoxP3+ regulatory T cells and significantly increased IL10 mRNA expression. This gnotobiotic model confirmed that Hb causes portal hepatitis in outbred SW mice but stimulated GALT with an antiinflammatory bias. Because Hb had both anti- and proinflammatory effects on GALT, it should be considered a 'pathosymbiont provocateur' and merits further evaluation in mouse models of human disease.
Insights
Helicobacter bilis causes liver inflammation and gut issues in mice. This bacterium stimulates the gut-associated lymphoid tissue (GALT) with both anti-inflammatory and pro-inflammatory effects.
Area of Science:
- Immunology
- Microbiology
- Hepatology
Background:
- Helicobacter bilis (Hb) is known to cause hepatitis in certain mouse strains.
- Previous studies indicated Hb's role in liver inflammation in conventional mice.
Purpose of the Study:
- To confirm Hb's direct role in causing portal hepatitis in outbred gnotobiotic Swiss Webster (SW) mice.
- To investigate Hb's impact on the gut-associated lymphoid tissue (GALT) and lower bowel immune responses.
Main Methods:
- Infection of gnotobiotic SW mice with Helicobacter bilis.
- Analysis of liver and lower bowel tissues at 1 and 10 months post-infection.
- Assessment of GALT hyperplasia, tertiary lymphoid tissue formation, and immune cell populations (B220+, CD4+ T cells) and cytokine mRNA expression (IL10).
Main Results:
- Hb infection directly caused portal hepatitis in gnotobiotic SW mice.
- Hb also induced mild enterocolitis, GALT expansion, and tertiary lymphoid tissue in the lower bowel.
- Hb-induced GALT showed features of tertiary lymphoid tissue and an anti-inflammatory bias with increased IL10 mRNA expression.
Conclusions:
- Helicobacter bilis is confirmed to cause portal hepatitis in outbred SW mice.
- Hb stimulates GALT with a mixed anti- and pro-inflammatory immune response, acting as a 'pathosymbiont provocateur'.
- This model warrants further investigation for its relevance to human diseases.
