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. 1977 Aug;17(2):430–438. doi: 10.1128/iai.17.2.430-438.1977

Suppression of babesiosis in BCG-infected mice and its correlation with tumor inhibition.

I A Clark, E J Wills, J E Richmond, A C Allison
PMCID: PMC421139  PMID: 330411

Abstract

Infection of mice with Bacillus Calmette-Guérin (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 Corynebactium 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.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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