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Related Concept Videos

Diversity of Protists II01:27

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Alveolates are a group of organisms recognized by the presence of alveoli, which are cytoplasmic sacs located beneath the cell membrane. While their function remains uncertain, alveoli may help regulate water balance by controlling how much water enters and leaves the cell. In dinoflagellates, these structures may serve as armor plates. There are three major types of alveolates: ciliates, which move using cilia; dinoflagellates, which use flagella for movement; and apicomplexans, which are...
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Detection of Plasmodium Sporozoites in Anopheles Mosquitoes using an Enzyme-linked Immunosorbent Assay
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Plasmodium falciparum picks (on) EPCR.

William C Aird1, Laurent O Mosnier, Rick M Fairhurst

  • 1The Center for Vascular Biology Research and.

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|November 20, 2013
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Summary

Cerebral malaria coma results from infected erythrocytes binding to EPCR, impairing the protein C system. This leads to inflammation and clotting in brain vessels, explaining this severe Plasmodium falciparum complication.

Area of Science:

  • Malariology
  • Pathogenesis of infectious diseases
  • Vascular biology

Background:

  • Cerebral malaria (CM) is a deadly complication of Plasmodium falciparum infection.
  • The precise mechanisms driving CM's organ-specific pathology, particularly coma, remain incompletely understood.
  • Understanding CM pathogenesis is crucial for developing targeted therapies.

Purpose of the Study:

  • To elucidate a novel mechanism underlying cerebral malaria pathogenesis.
  • To investigate the role of infected erythrocytes and endothelial protein C receptor (EPCR) in CM development.
  • To explore the link between EPCR function and the inflammatory state in CM.

Main Methods:

  • Analysis of data from two recent publications on CM.
  • Investigation of infected erythrocyte binding to EPCR.

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  • Assessment of EPCR depletion and its impact on the protein C system.
  • Evaluation of the resulting proinflammatory and procoagulant state in brain microvessels.

    • Main Results:

    • Infected erythrocytes express specific virulence proteins mediating binding to EPCR.
    • Malaria infection leads to the depletion of EPCR in brain microvessels.
    • EPCR depletion impairs the protein C system's anticoagulant and anti-inflammatory functions.
    • This impairment promotes a proinflammatory and procoagulant state conducive to CM.

    Conclusions:

    • A novel mechanism for CM pathogenesis involves IE binding to EPCR.
    • EPCR depletion and subsequent protein C system dysfunction are key events in CM.
    • This pathway contributes to the development of brain microvessel inflammation and thrombosis in CM.
    • Targeting the IE-EPCR interaction or the protein C pathway may offer therapeutic strategies for CM.