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Updated: Aug 30, 2026

Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice
12:48

Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice

Published on: January 2, 2013

[Pathogenesis of cerebral malaria: facts and hypotheses]

S C Wassmer1, N Coltel, V Combes

  • 1L'Unité de Parasitologie expérimentale, Laboratoire d'Immunopathologie, Faculté de Médecine, EA3282 UnivMed-IPP-IMTSSA, Marseille, France.

Medecine Tropicale : Revue Du Corps De Sante Colonial
|October 29, 2003
PubMed

Insights

Platelets accumulate in the brain during cerebral malaria (CM), a severe complication of Plasmodium falciparum infection. These platelets promote the adhesion of infected red blood cells to blood vessel walls, contributing to CM pathogenesis.

Area of Science:

  • Tropical medicine
  • Hematology
  • Immunology

Context:

  • Cerebral malaria (CM) is a severe Plasmodium falciparum complication characterized by infected red blood cell sequestration in cerebral vessels.
  • While metabolic and immune factors are implicated, the precise mechanisms of CM remain elusive.
  • Previous studies in mouse models suggested a role for host cells, particularly platelets.

Purpose:

  • To investigate the role of platelets in human cerebral malaria.
  • To determine if platelets contribute to the cytoadherence of parasitized red blood cells (PRBCs) in CM.

Summary:

  • Significantly higher platelet accumulation was observed in the cerebral capillaries and venules of Malawian patients who died from CM compared to those who died from other diseases.
  • Experiments demonstrated that platelets facilitate the adherence of PRBCs to endothelial cells (EC), even in the absence of CD36.
  • This platelet-mediated cytoadherence was shown to be resistant to physiological flow conditions, suggesting a crucial role in parasite sequestration.

Impact:

  • Establishes a link between platelet accumulation and parasite sequestration in cerebral malaria.
  • Highlights platelets as a key factor in the pathogenesis of CM.
  • Suggests potential therapeutic targets for preventing or treating CM by modulating platelet function or interaction with PRBCs.

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