TNF alpha, IL-1 and O2- release by macrophages do not correlate with the anti-mouse Hepatitis Virus 3 effect induced by interferon gamma
Microbial Pathogenesis
; 15(6): 447-454, 1993.
Article
in En
| SES-SP, SESSP-IBPROD, SES-SP, SESSP-IBACERVO
| ID: biblio-1064749
Responsible library:
BR78.1
Localization: BR78.1
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.
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Collection:
06-national
/
BR
Database:
SES-SP
/
SESSP-IBACERVO
/
SESSP-IBPROD
Main subject:
Murine hepatitis virus
/
Macrophage Activation
Limits:
Animals
Language:
En
Journal:
Microbial Pathogenesis
Year:
1993
Document type:
Article