The significance of alpha/beta interferons and gamma interferon produced in mice infected with Listeria monocytogenes

Abstract

Interferon (IFN)-α/β was induced in the circulation of mice infected intravenously with Listeria monocytogenes 24 to 72 hr after infection, but was not induced by the administration of heat-killed Listeria, listerial cell wall fraction (LCWF), or listerial soluble fraction. Appearance of IFN-α/β showed a pattern similar to that of the growth of bacteria in the spleen and the liver of mice. IFN-α/β production was abrogated by pretreatment of mice with anti-asialo GM1 antibody, antithymocyte serum, or hydrocortisone, but not with cyclophosphamide or carrageenan. Such treatments which suppressed IFN-α/β production did not influence bacterial growth in the organs of mice in the early stage of Listeria infection. Administration of IFN-α/β exogenously also did not. After 5 days of infection when the specific resistance against reinfection with Listeria was established, IFN-γ but not IFN-α/β was induced in the circulation 3 to 6 hr after stimulation with LCWF or reinfection with Listeria. IFN-γ production was abrogated completely by cyclophosphamide and antithymocyte serum, and partially by hydrocortisone and carrageenan, but not by anti-asialo GM1 antibody in Listeria-infected mice treated with these agents before induction of IFN-γ by LCWF. Presumably, IFN-α/β might be produced by asialo GM1-bearing cells but IFN-γ might not. However, IFN-γ production was suppressed in Listeria-infected mice, when IFN-α/β production had been inhibited by treatment with anti-asialo GM1 antibody or when the IFN produced had been neutralized with anti-mouse IFN-α/β antibody. Therefore, it is conceivable that IFN-α/β might be essential for the generation or the expression of antigen-specific T cells involving IFN-γ production and acquired resistance during Listeria infection. In fact, the bacterial growth in the organs of mice in the early stage of infection was normal in IFN-α/β-depleted mice but it resulted in the delay of T-cell-dependent elimination of bacteria from the organs of mice in the late stage.