No abstract

Tumor necrosis factor, lymphocyte-activating factor, and enhanced levels of type I interferon were found in serum samples taken 2 h after mice infected with Plasmodium vinckei subsp. petteri received a small intravenous injection of endotoxin. These three mediators are among those released when mice receive an endotoxin injection 2 weeks after Mycobacterium bovis BCG or Corynebacterium parvum have been administered. There is indirect evidence that this wider range of mediators is also released in P. vinckei subsp. petteri-infected mice given parenteral endotoxin. A recent report that endotoxin is detectable in the plasma of malaria-infected mice and children implies that these mediators may also be released in the acute phase of the natural infection. We propose that these macrophage-derived mediators may be important in the glucocorticoid antagonism, bone marrow depression, fever, hypergammaglobulinemia, splenomegaly, elevation of serum amyloid A, consumptive coagulopathy, and shock syndrome with associated organ damage which can accompany malaria. The intraerythrocytic parasite death seen at crisis in some malarias, as well as the subsequent development of specific protective immunity, may also depend on these mediators.

Mice which had been pre-treated with killedCorynebacterium parvumgiven intravenously or intraperitoneally, but not subcutaneously, were completely resistant ot infection withBabesia microtiorB. rodhaini, and protected from death caused byPlasmodium vinckeiorP. chabaudiinfection. There is evidence that the parasites died within circulating erythrocytes. This occurred much too soon for a specific antibody response to be evoked, and no antibody could be detected by the indirect fluorescent-anitbody technique. Thus it is suggested that a non-secific soluble mediator may play an important role in the protection observed.

No abstract

Infection of mice with Bacillus Calmette-Guerin (BCG) provided good protection against Babesia species. The intensity and duration of this protection was similar to that established after natural recovery from babesiosis. It developed too soon after the first exposure to the parasite, and was too radioresistant, to be attributable to specific antibody production. In addition, the parasites degenerated within circulating erythrocytes. This phenomenon is inconsistent with phagocytosis or lysis of parasites or parasitized cells, or prevention of entry of parasites into erythrocytes, causing the observed protection. Hence the phenomenon is best explained by the release of a nonspecific mediator that can limit multiplication of parasites within erythrocytes. These results not only throw light on mechanisms of immunity against hemoprotozoa. There are many points of similarity between the nonspecific protection BCG and Corynebacterium parvum provide against Babesia species and inhibition of tumor growth by these agents. Therefore, babesiosis in mice may be a convenient experimental model for assessing stimulation of the mononuclear phagocyte system, which appears to be the basis of nonspecific immunity against bacteria, parasites, and tumors.