Lipopolysaccharide-sensitivity of interferon-γ receptor deficient mice

Abstract

Interteron-γ receptor deficient (IFNγR-/-) and control wild-type (IFNγR+/+) mice were compared for their susceptibility to lipopolysaccharide (LPS) and tumor necrosis factor α (TNFα) before and after treatment with the LPSsensitizing agents D-galactosamine (D-GalN) or Propionibacterium acnes. Untreated and D-GalN-sensitized, IFNγR-/and IFNγR+/+ mice were comparable in their TNFα responses to LPS. Deficient and wild-type mice also exhibited a similar susceptibility to the lethal effects of LPS or TNFα which was enhanced by D-GalN treatment to a comparable extent. After treatment with P. acnes, the LPS and TNFα responsiveness remained unchanged in IFNγR-/- mice while in IFNγR+/+ mice they were enhanced up to 200-fold. These results indicate that IFN-γ mediates the LPS and TNFα hypersensitivity of P. acnes treated mice, while the normal sensitivity to LPS or TNFα in the presence or absence of D-GalN is IFN-γ independent.