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Protective effects of macrophage-derived interferon against encephalomyocarditis virus-induced diabetes mellitus in
K Hirasawa1, Y Ogiso, M Takeda
1Department of Biomedical Science, Faculty of Agriculture, University of Tokyo, Japan.
Abstract:
The involvement of macrophages in protection against diabetes mellitus in mice of BALB/c (susceptible) and C57BL (resistant) strains infected with the B (non-diabetogenic) or D (highly diabetogenic) variant of encephalomyocarditis (EMC) virus was examined. Pretreatment with the B variant of EMC virus (EMC-B), avirulent interferon (IFN) inducer, or Corynebacterium parvum inhibited diabetes in BALB/c mice infected with the D variant of EMC virus (EMC-D). Treatment of C57BL mice with carrageenan to compromise macrophage function rendered C57BL mice susceptible to EMC-D-induced diabetes. In macrophage culture for BALB/c mice, EMC-B induced IFN at an earlier stage than did EMC-D. The C57BL mouse-derived macrophages produced more IFN than did BALB/c mouse-derived macrophages after stimulation with EMC-D. Moreover, C. parvum increased IFN production in macrophage cultures from BALB/c mice, whereas carrageenan inhibited that in macrophage cultures from C57BL mice. These results suggest that IFN derived from macrophages may have an important role in protecting mice against EMC virus infection.
Insights
Macrophages protect against diabetes mellitus induced by encephalomyocarditis virus (EMC-D) in mice. Interferon (IFN) produced by macrophages plays a key role in this protective immune response.
Area of Science:
- Immunology
- Virology
- Pathology
Background:
- Macrophages are crucial immune cells involved in host defense.
- Diabetes mellitus can be induced by certain viral infections, such as encephalomyocarditis virus (EMC).
- Genetic background (e.g., BALB/c vs. C57BL mice) influences susceptibility to viral infections and disease development.
Purpose of the Study:
- To investigate the role of macrophages in protection against EMC virus-induced diabetes mellitus.
- To compare the macrophage response in susceptible (BALB/c) and resistant (C57BL) mouse strains.
- To elucidate the involvement of interferon (IFN) in this process.
Main Methods:
- Mice of BALB/c and C57BL strains were infected with diabetogenic (EMC-D) or non-diabetogenic (EMC-B) EMC virus variants.
- Macrophage function was modulated using EMC-B virus, Corynebacterium parvum, or carrageenan.
- Interferon production by macrophages in vitro was measured following viral stimulation.
Main Results:
- Pretreatment with EMC-B or Corynebacterium parvum protected susceptible BALB/c mice from EMC-D-induced diabetes.
- Compromising macrophage function with carrageenan rendered resistant C57BL mice susceptible to EMC-D.
- Macrophages from resistant C57BL mice produced more IFN than those from susceptible BALB/c mice upon EMC-D stimulation.
- Corynebacterium parvum enhanced IFN production in BALB/c macrophages, while carrageenan inhibited it in C57BL macrophages.
Conclusions:
- Macrophages play a significant role in protecting against EMC virus-induced diabetes.
- Interferon derived from macrophages is likely a key mediator of this protection.
- The differential IFN production capacity of macrophages from resistant versus susceptible mouse strains contributes to varying disease outcomes.