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Macrophages in mice acutely infected with lymphocytic choriomeningitis virus are primed for nitric oxide synthesis
E A Butz1, B S Hostager, P J Southern
1Department of Microbiology, University of Minnesota Medical School, Minneapolis 55455.
Abstract:
Following infection of adult mice with lymphocytic choriomeningitis virus (LCMV) there is a well documented suppression of T-cell and B-cell functions concurrent with the strong anti-LCMV immune response. Macrophages have been shown to be infected and activated during acute LCMV infection and there is some evidence to indicate that there is altered antigen presentation in acutely infected mice. We have examined nitric oxide (NO) production by splenic macrophages during acute infection of adult mice. Our results show that these macrophages are primed for production of NO, that the inducible production of NO parallels the immune suppression, and that NO production is dependent on the presence of IFN gamma. However, neither in vivo nor in vitro treatment with N-monomethyl-L-arginine (NMA), a specific inhibitor of nitric oxide synthase, altered the induction or maintenance of virus-induced immune suppression in mice acutely infected with LCMV.
Insights
Lymphocytic choriomeningitis virus (LCMV) infection in mice suppresses T and B cell functions. While nitric oxide (NO) production by macrophages correlates with this suppression, inhibiting NO did not affect LCMV-induced immune suppression.
Area of Science:
- Immunology
- Virology
- Cellular Biology
Background:
- Adult mice infected with lymphocytic choriomeningitis virus (LCMV) exhibit suppressed T-cell and B-cell functions alongside a robust anti-LCMV immune response.
- Macrophages are infected and activated during acute LCMV infection, with evidence suggesting altered antigen presentation.
- The role of nitric oxide (NO) in LCMV-induced immune suppression requires further investigation.
Purpose of the Study:
- To investigate nitric oxide (NO) production by splenic macrophages during acute LCMV infection in adult mice.
- To determine the correlation between inducible NO production and immune suppression.
- To assess the impact of nitric oxide synthase inhibition on LCMV-induced immune suppression.
Main Methods:
- Analysis of nitric oxide (NO) production by splenic macrophages from adult mice acutely infected with LCMV.
- Assessment of NO production dependence on interferon-gamma (IFN-γ).
- In vivo and in vitro experiments using N-monomethyl-L-arginine (NMA), a nitric oxide synthase inhibitor.
Main Results:
- Splenic macrophages from LCMV-infected mice are primed for NO production.
- Inducible NO production by macrophages parallels the observed immune suppression.
- NO production is dependent on the presence of IFN-γ.
- Inhibition of NO production using NMA did not alter the induction or maintenance of virus-induced immune suppression.
Conclusions:
- Macrophages in LCMV-infected mice produce nitric oxide (NO) in correlation with immune suppression.
- Interferon-gamma (IFN-γ) is essential for inducible NO production.
- Despite the correlation, NO production is not the primary mechanism driving LCMV-induced immune suppression in T and B cells.