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Parenteral injection of dextran sulfate 500 (DS 500; 50 mg/kg of body weight) into mice caused a complete loss of resistance to a sublethal (2 X 10(3) to 5 X 10(3)) infection with Listeria monocytogenes. Such loss could be prevented by pretreatment of animals with 3 X 10(9) heat-killed Bordetella pertussis organisms (PO) 5 to 30 days before the administration of DS 500. The increased phagocytic capcity induced by PO was only exhausted when a fourfold dose of DS 500, effecting complete loss of antibacterial resistance (50 mg/kg ob body weight), was administered. Listeriosis in mice treated with DS 500 is characterized by rapid-progressive necro-purulent inflammation of liver and spleen, lack of mononuclear phagocyte response, and 100% lethality within 72 h after infection. In contrast, the time course, extent, and morphological characteristics of listeriosis in animals pretreated with PO before the DS 500 application were not significantly different from those of nonpretreated controls. Evidence is presented that the protective effect of PO is due to activation of the mononuclear phagocyte system, which without such treatment is blocked by the DS 500 administration. The data presented indicate that the protective effect of PO is due only in part to the endotoxic moiety of these bacteria. Differences in the course and morphology of listeriosis in animals with dysfunction of the mononuclear phagocyte system and in animals with deficiency of the cellular immune system are discussed.

Reversion of dextran sulfate-induced loss of antibacterial resistance by Bordetella pertussis