Murine amebiasis: the role of the macrophage in host defense.
The congenitally athymic nude (nu/nu) mouse was studied as a model for amebic liver disease, using Entamoeba histolytica. Despite intrahepatic inoculation of massive numbers of amebae, we could not produce sustained infections in nu/nu mice. We also failed to induce hepatic amebiasis in thymus-intact nu/+ and +/+ littermates, or in nu/+ mice pretreated with rabbit antimouse thymocyte globulin. Humoral response was measured in both the nu/nu and nu/+ mice. Nu/+ but not nu/nu animals developed a specific IgG response after challenge with E. histolytica. There were no significant IgM responses. Pretreatment with silica increased susceptibility of both nu/nu and nu/+ mice to development of liver abscesses. These studies suggest that host resistance in murine amebiasis is critically dependent upon the macrophage, but not upon T cell-mediated defenses.
D000818:Animals; D000961:Antilymphocyte Serum / Q000494:pharmacology; D004748:Entamoeba histolytica / Q000276:immunology; D005856:Germ-Free Life; D007113:Immunity, Innate; D007074:Immunoglobulin G / Q000096:biosynthesis; D007075:Immunoglobulin M / Q000096:biosynthesis; D008101:Liver Abscess, Amebic / Q000276:immunology*; D008264:Macrophages / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D012822:Silicon Dioxide / Q000494:pharmacology; D013601:T-Lymphocytes / Q000276:immunology
D000961:Antilymphocyte Serum; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D012822:Silicon Dioxide