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Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice
Published on: January 2, 2013
Young Sprague Dawley rats infected by Plasmodium berghei: A relevant experimental model to study cerebral malaria
Sokhna Keita Alassane1,2,3, Marie-Laure Nicolau-Travers1,2, Sandie Menard4
1CNRS, LCC (Laboratoire de Chimie de Coordination), 205 route de Narbonne, Toulouse, France.
Abstract:
Cerebral malaria (CM) is the most severe manifestation of human malaria yet is still poorly understood. Mouse models have been developed to address the subject. However, their relevance to mimic human pathogenesis is largely debated. Here we study an alternative cerebral malaria model with an experimental Plasmodium berghei Keyberg 173 (K173) infection in Sprague Dawley rats. As in Human, not all infected subjects showed cerebral malaria, with 45% of the rats exhibiting Experimental Cerebral Malaria (ECM) symptoms while the majority (55%) of the remaining rats developed severe anemia and hyperparasitemia (NoECM). These results allow, within the same population, a comparison of the noxious effects of the infection between ECM and severe malaria without ECM. Among the ECM rats, 77.8% died between day 5 and day 12 post-infection, while the remaining rats were spontaneously cured of neurological signs within 24-48 hours. The clinical ECM signs observed were paresis quickly evolving to limb paralysis, global paralysis associated with respiratory distress, and coma. The red blood cell (RBC) count remained normal but a drastic decrease of platelet count and an increase of white blood cell numbers were noted. ECM rats also showed a decrease of glucose and total CO2 levels and an increase of creatinine levels compared to control rats or rats with no ECM. Assessment of the blood-brain barrier revealed loss of integrity, and interestingly histopathological analysis highlighted cyto-adherence and sequestration of infected RBCs in brain vessels from ECM rats only. Overall, this ECM rat model showed numerous clinical and histopathological features similar to Human CM and appears to be a promising model to achieve further understanding the CM pathophysiology in Humans and to evaluate the activity of specific antimalarial drugs in avoiding/limiting cerebral damages from malaria.
Insights
This study introduces a new rat model for cerebral malaria (CM), a severe form of malaria. The model effectively mimics human CM symptoms and pathology, offering a valuable tool for research.
Area of Science:
- Parasitology
- Neurology
- Pathophysiology
Background:
- Cerebral malaria (CM) is a severe malaria complication with poorly understood pathogenesis.
- Existing mouse models for CM have limitations in mimicking human disease.
- There is a need for better models to study CM and test potential treatments.
Purpose of the Study:
- To evaluate a novel experimental cerebral malaria (ECM) model using Plasmodium berghei K173 infection in Sprague Dawley rats.
- To compare the pathological effects of ECM versus severe malaria without neurological symptoms (NoECM) within the same population.
- To assess the clinical and histopathological relevance of this rat model to human CM.
Main Methods:
- Induction of experimental cerebral malaria (ECM) in Sprague Dawley rats via Plasmodium berghei K173 infection.
- Monitoring of clinical signs, survival rates, and hematological parameters (platelets, white blood cells).
- Biochemical analysis (glucose, CO2, creatinine) and assessment of blood-brain barrier integrity and brain histopathology.
Main Results:
- 45% of infected rats developed ECM, while 55% had severe anemia/hyperparasitemia (NoECM).
- ECM rats exhibited neurological symptoms (paralysis, respiratory distress, coma), with 77.8% mortality; survivors recovered rapidly.
- ECM rats showed decreased glucose/CO2, increased creatinine, blood-brain barrier disruption, and sequestration of infected RBCs in brain vessels.
Conclusions:
- The Sprague Dawley rat model infected with P. berghei K173 exhibits significant clinical and histopathological similarities to human cerebral malaria.
- This model allows for direct comparison between ECM and severe malaria without neurological involvement.
- The model is a promising tool for advancing the understanding of CM pathophysiology and for evaluating antimalarial drugs targeting cerebral damage.
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