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Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice
Published on: January 2, 2013
Genetic analysis of cerebral malaria in the mouse model infected with Plasmodium berghei
Sabrina Torre1, David Langlais1,2, Philippe Gros3,4
1Department of Biochemistry, Department of Human Genetics, McGill University Research Centre on Complex Traits, McGill University, Montreal, QC, Canada.
Abstract:
Malaria is a common and sometimes fatal disease caused by infection with Plasmodium parasites. Cerebral malaria (CM) is a most severe complication of infection with Plasmodium falciparum parasites which features a complex immunopathology that includes a prominent neuroinflammation. The experimental mouse model of cerebral malaria (ECM) induced by infection with Plasmodium berghei ANKA has been used abundantly to study the role of single genes, proteins and pathways in the pathogenesis of CM, including a possible contribution to neuroinflammation. In this review, we discuss the Plasmodium berghei ANKA infection model to study human CM, and we provide a summary of all host genetic effects (mapped loci, single genes) whose role in CM pathogenesis has been assessed in this model. Taken together, the reviewed studies document the many aspects of the immune system that are required for pathological inflammation in ECM, but also identify novel avenues for potential therapeutic intervention in CM and in diseases which feature neuroinflammation.
Insights
The experimental mouse model of cerebral malaria (ECM) aids in understanding malaria complications. This review summarizes host genetic factors influencing ECM pathogenesis and neuroinflammation, revealing therapeutic targets.
Area of Science:
- Immunology
- Neuroscience
- Parasitology
Background:
- Malaria, caused by Plasmodium parasites, can be fatal.
- Cerebral malaria (CM) is a severe complication of Plasmodium falciparum infection, characterized by neuroinflammation.
- The experimental mouse model of cerebral malaria (ECM) using Plasmodium berghei ANKA is a key tool for studying CM pathogenesis.
Purpose of the Study:
- To review the utility of the Plasmodium berghei ANKA mouse model for studying human CM.
- To summarize host genetic factors influencing CM pathogenesis and neuroinflammation within the ECM model.
- To identify potential therapeutic targets for CM and other neuroinflammatory diseases.
Main Methods:
- Review of existing literature on the Plasmodium berghei ANKA infection model.
- Compilation and analysis of studies assessing host genetic effects (loci, genes) in ECM pathogenesis.
- Synthesis of findings related to immune system involvement in ECM and neuroinflammation.
Main Results:
- The ECM model effectively recapitulates key aspects of CM immunopathology, including neuroinflammation.
- Numerous host genetic factors and immune pathways have been implicated in ECM pathogenesis.
- Studies highlight the complex interplay between the host immune system and parasite in driving disease.
Conclusions:
- The Plasmodium berghei ANKA mouse model is invaluable for dissecting CM pathogenesis and neuroinflammation.
- Understanding host genetic contributions provides insights into disease mechanisms.
- This research identifies potential therapeutic strategies for CM and neuroinflammatory conditions.
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