Host defenses in murine malaria: analysis of plasmodial infection-caused defects in macrophage microbicidal capacities.
Macrophage-dependent killing of facultative intracellular bacteria was markedly impaired by overt erythrocytic Plasmodium yoelii or Plasmodium berghei infection of mice. P. yoelii infection was capable of ablating not only the macrophage microbicidal capacity of "normal" animals but also the bactericidal capacities of "activated" macrophages. The uptake by spleen and liver of an intravenous challenge of Listeria monocytogenes was not altered by plasmodial infection, but within hours of injection markedly enhanced bacterial growth was found in tissues of malarious mice. The evidence gives credence to the view that the uptake of bacteria by macrophages of malarious mice was normal but that malarious mice, unlike normal mice, were unable to kill the bacteria. The plasmodial infection-caused defect in macrophage microbicidal capacity could be partially mimicked by the intravenous injection of large numbers of nonreplicating heterologous particles (i.e., killed bacteria, sheep erythrocytes). This result suggests that the uptake of particles generated during overt erythrocytic malaria may be responsible for the malaria-associated defects in macrophage bactericidal capacity.
D000818:Animals; D001419:Bacteria / Q000254:growth & development*; D001424:Bacterial Infections / Q000276:immunology*; D005260:Female; D007111:Immunity, Cellular; D008088:Listeriosis / Q000276:immunology; D008264:Macrophages / Q000276:immunology* / Q000382:microbiology; D008288:Malaria / Q000276:immunology*; D051379:Mice; D010587:Phagocytosis; D010962:Plasmodium berghei