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Immunization against cerebral pathology inPlasmodium berghei-infected mice

J. H. A. J. Curfs, Cornelis C. Hermsen, Joep H.E.Th. Meuwissen, Wijnand M. C. Eling

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Abstract

The development of cerebral lesions in Plasmodium berghei-infected mice was dependent on the strain of mice and the size of the infectious inoculum. In particular, C57Bl/6J mice develop cerebral lesions when infected with low numbers of parasitized erythrocytes. By increasing the number of parasites in the infectious inoculum, the percentage of animals that develop cerebral malaria is decreased. Varying degrees of protection against the development of cerebral malaria can be obtained by several methods of immunization. (1) Injection of mice with large numbers of disrupted parasitized erythrocytes 1 or 2 weeks before the challenge infection (protection up to 70%). (2) A 2-day immunizing infection given 9 or 14 days before the challenge infection (protection up to 85%). (3) Injection of mice with plasmodial exoantigen preparations 1 week before the challenge infection (variable protection-rate, up to 100%). In all mice protected against cerebral malaria, parasitaemia is not affected by the immunizing treatment, indicating that protective mechanisms against cerebral malaria and parasitaemia are independent.

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What this paper is about

The development of cerebral lesions in Plasmodium berghei-infected mice was dependent on the strain of mice and the size of the infectious inoculum. In particular, C57Bl/6J mice develop cerebral lesions when infected with low numbers of parasitized erythrocytes. By increasing the number of parasites in the infectious inoculum, the percentage of animals that develop cerebral malaria is decreased. Varying degrees of protection against the development of cerebral malaria can be obtained by several methods of immunization. (1) Injection of mice with large numbers of disrupted parasitized erythrocytes 1 or 2 weeks before the challenge infection (protection up to 70%). (2) A 2-day immunizing infection given 9 or 14 days before the challenge infection (protection up to 85%). (3) Injection of mice with plasmodial exoantigen preparations 1 week before the challenge infection (variable protection-rate, up to 100%). In all mice protected against cerebral malaria, parasitaemia is not affected by the immunizing treatment, indicating that protective mechanisms against cerebral malaria and parasitaemia are independent.

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Available abstract

The development of cerebral lesions in Plasmodium berghei-infected mice was dependent on the strain of mice and the size of the infectious inoculum. In particular, C57Bl/6J mice develop cerebral lesions when infected with low numbers of parasitized erythrocytes. By increasing the number of parasites in the infectious inoculum, the percentage of animals that develop cerebral malaria is decreased. Varying degrees of protection against the development of cerebral malaria can be obtained by several methods of immunization. (1) Injection of mice with large numbers of disrupted parasitized erythrocytes 1 or 2 weeks before the challenge infection (protection up to 70%). (2) A 2-day immunizing infection given 9 or 14 days before the challenge infection (protection up to 85%). (3) Injection of mice with plasmodial exoantigen preparations 1 week before the challenge infection (variable protection-rate, up to 100%). In all mice protected against cerebral malaria, parasitaemia is not affected by the immunizing treatment, indicating that protective mechanisms against cerebral malaria and parasitaemia are independent.

Key concepts: Plasmodium berghei, Cerebral Malaria, Malaria, Biology, Immunization, Immunology, Virology, Parasitemia

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