The significance of alpha/beta interferons and gamma interferon produced in mice infected with Listeria monocytogenes.
Interferon (IFN)-alpha/beta 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-alpha/beta showed a pattern similar to that of the growth of bacteria in the spleen and the liver of mice. IFN-alpha/beta 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-alpha/beta production did not influence bacterial growth in the organs of mice in the early stage of Listeria infection. Administration of IFN-alpha/beta exogenously also did not. After 5 days of infection when the specific resistance against reinfection with Listeria was established, IFN-gamma but not IFN-alpha/beta was induced in the circulation 3 to 6 hr after stimulation with LCWF or reinfection with Listeria. IFN-gamma 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-gamma by LCWF. Presumably, IFN-alpha/beta might be produced by asialo GM1-bearing cells but IFN-gamma might not. However, IFN-gamma production was suppressed in Listeria-infected mice, when IFN-alpha/beta production had been inhibited by treatment with anti-asialo GM1 antibody or when the IFN produced had been neutralized with anti-mouse IFN-alpha/beta antibody. Therefore, it is conceivable that IFN-alpha/beta might be essential for the generation or the expression of antigen-specific T cells involving IFN-gamma 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-alpha/beta-depleted mice but it resulted in the delay of T-cell-dependent elimination of bacteria from the organs of mice in the late stage.
D000818:Animals; D005677:G(M1) Ganglioside / Q000276:immunology; D006028:Glycosphingolipids / Q000276:immunology; D007166:Immunosuppressive Agents / Q000494:pharmacology; D007370:Interferon Type I / Q000276:immunology*; D007371:Interferon-gamma / Q000276:immunology*; D007372:Interferons / Q000096:biosynthesis; D008088:Listeriosis / Q000276:immunology* / Q000382:microbiology; D008099:Liver / Q000382:microbiology; D051379:Mice; D013154:Spleen / Q000382:microbiology; D013601:T-Lymphocytes / Q000276:immunology; D013997:Time Factors
D006028:Glycosphingolipids; D007166:Immunosuppressive Agents; D007370:Interferon Type I; D005677:G(M1) Ganglioside; D007371:Interferon-gamma; D007372:Interferons