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TNF alpha, IL-1 and O2- release by macrophages do not correlate with the anti-mouse hepatitis virus 3 effect induced
M A Lucchiari1, M Modolell, R C Vassão
1Instituto Butantan, Laboratorio de Imunologia Viral, S. Paulo, Brasil.
Abstract:
Macrophages have been described to be important in determining the resistance of A/J mice or the susceptibility of BALB/c mice to the experimental infection with Mouse Hepatitis Virus 3 (MHV3). The interferon gamma (IFN gamma) activation of A/J and BALB/c mouse macrophages was shown to partially restrict the MHV3 replication only in macrophages from the resistant A/J mice. The activation by IFN gamma and/or infection with MHV3 showed that BALB/c mouse macrophages were capable of releasing tumor necrosis factor alpha (TNF alpha), interleukin 1 (IL-1) and anion superoxide (O2-), and A/J mouse macrophages were capable of releasing TNF alpha and IL-1 but not O2-. Comparable amounts of TNF alpha or IL-1 were released by IFN gamma-activated A/J or BALB/c mouse macrophages. Following MHV3 infection or IFN gamma activation and MHV3 infection, BALB/c mouse macrophages were always capable of releasing higher amounts of TNF alpha, IL-1 or O2- than A/J mouse macrophages, which correlated with their susceptibility to the virus infection. The data indicate that the anti-MHV3 effect induced by IFN gamma in A/J mouse macrophages is not related to the studied extrinsic activities of these cells.
Insights
Mouse macrophages exhibit different responses to Mouse Hepatitis Virus 3 (MHV3). Interferon gamma (IFN gamma) partially restricts MHV3 in resistant A/J mice but not susceptible BALB/c mice, indicating distinct immune mechanisms.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Macrophages play a key role in determining host resistance or susceptibility to Mouse Hepatitis Virus 3 (MHV3).
- Previous studies suggest differential responses of A/J (resistant) and BALB/c (susceptible) mouse macrophages to MHV3 infection.
Purpose of the Study:
- To investigate the role of interferon gamma (IFN gamma) activation on MHV3 replication in macrophages from resistant A/J and susceptible BALB/c mice.
- To compare the cytokine and reactive oxygen species production by activated macrophages from these mouse strains upon MHV3 infection.
Main Methods:
- Macrophages from A/J and BALB/c mice were activated with IFN gamma and/or infected with MHV3.
- MHV3 replication was assessed.
- Production of tumor necrosis factor alpha (TNF alpha), interleukin-1 (IL-1), and superoxide anion (O2-) was measured.
Main Results:
- IFN gamma partially restricted MHV3 replication only in A/J mouse macrophages.
- BALB/c macrophages released higher amounts of TNF alpha, IL-1, and O2- compared to A/J macrophages after IFN gamma activation and/or MHV3 infection.
- Comparable levels of TNF alpha and IL-1 were released by IFN gamma-activated macrophages from both strains, but O2- production differed significantly.
Conclusions:
- The anti-MHV3 effect of IFN gamma in A/J macrophages is not linked to the measured extracellular activities (TNF alpha, IL-1, O2-).
- Differential production of inflammatory mediators by macrophages correlates with the susceptibility of mouse strains to MHV3 infection.
- These findings highlight distinct macrophage functional phenotypes contributing to viral resistance and susceptibility.