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Updated: Aug 20, 2026
The Citrobacter rodentium Mouse Model: Studying Pathogen and Host Contributions to Infectious Colitis
Published on: February 19, 2013
Pathogenicity of Helicobacter rodentium in A/JCr and SCID mice
Matthew H Myles1, Robert S Livingston, Craig L Franklin
1Research Animal Diagnostic Laboratory, Department of Veterinary Pathobiology, University of Missouri, Columbia, Missouri, USA.
Abstract:
Helicobacter rodentium was first recognized as a potential pathogen when it was isolated, along with Helicobacter bilis, from a colony of scid/Trp53 knockout mice with diarrhea. Clinical disease in these mice was more severe than that previously reported in mice infected with H. bilis alone, thus suggesting that H. rodentium contributed to the pathogenesis of enteritis. The purpose of the study reported here was to address two questions: is H. rodentium pathogenic in mice, and when co-infection with a pathogenic helicobacter occurs, does H. rodentium augment disease? To this end, A/JCr and C.B-17/IcrCrl-scidBr mice were inoculated with H. rodentium and/or H. hepaticus. Twelve weeks after inoculation, mice were euthanized. The cecum and liver were evaluated microscopically for evidence of disease. Cecal interferon-inducible protein 10 (IP-10), macrophage inflammatory protein 1alpha (MIP-1alpha), interleukin 10 (IL-10), and interferon gamma (IFN-gamma) mRNA values were measured as an indicator of mucosal immune response. Hepatic lesions were not identified in mice mono-infected with H. rodentium; likewise, cecal lesion scores were not significantly different from those of uninfected controls. With the exception of an increased IL-10 mRNA value in SCID mice, mean immune-related gene expression in H. rodentium mono-infected and uninfected control mice was not significantly different. In contrast, all mice infected with H. hepaticus developed moderate to severe hepatitis, significant increase in cecal lesion scores, and increased immune-related gene expression. The C.B-17/IcrCrl-scidBr mice co-infected with H. hepaticus and H. rodentium had liquid cecal contents and low terminal body weight. Further, compared with mice infected with H. hepaticus alone, co-infection was associated with significant increases of IL-10, MIP-1alpha, and IP-10 mRNA values in C.B-17/IcrCrl-scidBr and IFN-gamma and MIP-1alpha mRNA values in A/JCr mice. These results suggested that H. rodentium alone does not cause hepatitis or enteritis in A/JCr or C.B-17/IcrCrl-scidBr mice; however, co-infection with H. hepaticus and H. rodentium was associated with augmented cecal gene expression and clinical manifestation of disease in immunodeficient mice.
Insights
Helicobacter rodentium does not cause disease alone but can worsen enteritis when co-infecting mice with Helicobacter hepaticus. This study investigated H. rodentium's pathogenicity and its role in augmenting disease during co-infection.
Area of Science:
- Microbiology
- Immunology
- Gastroenterology
Background:
- Helicobacter rodentium was initially identified as a potential pathogen in immunocompromised mice exhibiting diarrhea.
- Co-infection with H. rodentium and H. bilis resulted in more severe disease than H. bilis alone, suggesting H. rodentium's contribution to enteritis pathogenesis.
Purpose of the Study:
- To determine if Helicobacter rodentium is pathogenic in mice.
- To investigate whether H. rodentium augments disease severity during co-infection with a pathogenic Helicobacter species.
Main Methods:
- Mice (A/JCr and C.B-17/IcrCrl-scidBr) were inoculated with H. rodentium and/or H. hepaticus.
- Cecal and liver tissues were microscopically examined for disease.
- Cecal mRNA levels of immune-related genes (IP-10, MIP-1alpha, IL-10, IFN-gamma) were quantified.
Main Results:
- H. rodentium mono-infection did not cause significant hepatic or cecal lesions or alter immune gene expression compared to controls.
- H. hepaticus infection led to moderate to severe hepatitis, increased cecal lesions, and elevated immune gene expression.
- Co-infection with H. hepaticus and H. rodentium in immunodeficient mice exacerbated clinical signs (liquid cecal contents, low body weight) and significantly increased cecal immune gene expression.
Conclusions:
- Helicobacter rodentium is not pathogenic on its own in the studied mouse models.
- Co-infection with H. hepaticus and H. rodentium significantly augments disease severity and mucosal immune responses in immunodeficient mice.
