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Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
Infection with murine norovirus 4 does not alter Helicobacter-induced inflammatory bowel disease in Il10(-/-) mice
Charlie C Hsu1, Jisun Paik2, Piper M Treuting2
1Department of Comparative Medicine, University of Washington, Seattle, Washington, USA. chuckhsu@uw.edu.
Abstract:
Infection of laboratory mice with murine noroviruses (MNV) is widely prevalent. MNV alters various mouse models of disease, including the Helicobacter bilis-induced mouse model of inflammatory bowel disease (IBD) in Mdr1a(--) mice. To further characterize the effect of MNV on IBD, we used mice deficient in the immunoregulatory cytokine IL10 (Il10(-/-) mice). In vitro infection of Il10(-/-) bone marrow-derived macrophages (BMDM) with MNV4 cocultured with H. bilis antigens increased the gene expression of the proinflammatory cytokines IL1β, IL6, and TNFα as compared with that of BMDM cultured with H. bilis antigens only. Therefore, to test the hypothesis that MNV4 infection increases inflammation and alters disease phenotype in H. bilis-infected Il10(-/-) mice, we compared the amount and extent of inflammation in Il10(-/-) mice coinfected with H. bilis and MNV4 with those of mice singly infected with H. bilis. IBD scores, incidence of IBD, or frequency of severe IBD did not differ between mice coinfected with H. bilis and MNV4 and those singly infected with H. bilis. Mice infected with MNV4 only had no appreciable IBD, comparable to uninfected mice. Our findings suggest that, unlike in Mdr1a(-/-) mice, the presence of MNV4 in Il10(-/-) mouse colonies is unlikely to affect the IBD phenotype in a Helicobacter-induced model. However, because MNV4 altered cytokine expression in vitro, our results highlight the importance of determining the potential influence of MNV on mouse models of inflammatory disease, given that MNV has a tropism for macrophages and dendritic cells and that infection is widely prevalent.
Insights
Murine norovirus (MNV) infection did not worsen inflammatory bowel disease (IBD) in IL-10 deficient mice, despite altering inflammatory cytokine expression in vitro. This suggests MNV may not impact this specific Helicobacter-induced IBD model.
Area of Science:
- Immunology
- Microbiology
- Gastroenterology
Background:
- Murine norovirus (MNV) is a prevalent infection in laboratory mice.
- MNV can influence various disease models, including Helicobacter bilis-induced inflammatory bowel disease (IBD) in Mdr1a(-/-) mice.
- The impact of MNV on IBD in IL-10 deficient (Il10(-/-)) mice requires further investigation.
Purpose of the Study:
- To determine if MNV4 infection exacerbates inflammation and alters the disease phenotype in H. bilis-infected Il10(-/-) mice.
- To assess the effect of MNV4 on cytokine expression in macrophages in vitro.
- To evaluate the potential influence of MNV on mouse models of inflammatory disease.
Main Methods:
- In vitro infection of Il10(-/-) bone marrow-derived macrophages (BMDM) with MNV4 and H. bilis antigens.
- Comparison of gene expression of proinflammatory cytokines (IL1β, IL6, TNFα).
- In vivo comparison of IBD scores, incidence, and severity in Il10(-/-) mice coinfected with H. bilis and MNV4 versus singly infected with H. bilis.
Main Results:
- In vitro, MNV4 infection with H. bilis antigens increased proinflammatory cytokine gene expression in BMDM compared to H. bilis antigens alone.
- In vivo, IBD scores, incidence, or severity did not differ between coinfected and singly infected Il10(-/-) mice.
- Mice infected with MNV4 alone showed no significant IBD.
Conclusions:
- MNV4 infection is unlikely to affect the IBD phenotype in a Helicobacter-induced model in Il10(-/-) mice, unlike in Mdr1a(-/-) mice.
- Despite no observed in vivo effect on IBD phenotype, MNV4's in vitro impact on cytokine expression highlights the need to consider MNV's influence on inflammatory disease models.
- The tropism of MNV for macrophages and dendritic cells underscores the importance of accounting for widespread MNV infections in research settings.
