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Related Experiment Video

Updated: May 18, 2026

Methods to Investigate the Regulatory Role of Small RNAs and Ribosomal Occupancy of Plasmodium falciparum

Methods to Investigate the Regulatory Role of Small RNAs and Ribosomal Occupancy of Plasmodium falciparum

Published on: December 4, 2015

Pathogenesis of malaria revisited.

Prasad Dasari¹, Sucharit Bhakdi

¹Institute of Medical Microbiology and Hygiene, University Medical Center, Johannes Gutenberg University Mainz, Hochhaus Augustusplatz, 55101 Mainz, Germany.

Medical Microbiology and Immunology

|September 8, 2012

Summary

The malaria parasite's digestive vacuole (DV) membrane triggers blood's complement and coagulation systems, contributing to severe malaria pathology. Dextran sulfate can suppress this dual activation, offering a potential therapeutic avenue.

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Area of Science:

Pathobiology
Malaria Pathogenesis
Immunology

Background:

Plasmodium falciparum malaria causes over a million deaths annually.
Parasitemia levels can be extremely high during infection.
The parasite's digestive vacuole (DV) processes hemoglobin, producing hemozoin (malaria pigment).

Purpose of the Study:

To investigate whether digestive vacuoles (DVs) released into the bloodstream trigger pathobiological events.
To identify the common trigger for complement and coagulation activation observed in severe malaria.
To explore the potential of DV membrane as a determinant of parasite pathogenicity.

Main Methods:

Investigated the capacity of the DV membrane to activate complement and coagulation cascades.
Assessed the effect of low-molecular-weight dextran sulfate on DV-induced activation.
Evaluated the impact of DV phagocytosis on immune cells (PMNs) in experimental models.

Main Results:

The DV membrane, but not the merozoite, spontaneously activates the alternative complement and intrinsic clotting pathways.
DV ejection leads to selective opsonization and phagocytosis of the DV, while merozoites remain free.
The DV membrane assembles prothrombinase, a key component of the intrinsic clotting pathway.
Low-molecular-weight dextran sulfate suppresses the dual activation capacity of the DV and protects animals.
Phagocytosis of DVs exhausts immune cells, potentially increasing susceptibility to bacterial infections.

Conclusions:

The digestive vacuole (DV) membrane is a significant trigger for both complement and coagulation activation in the blood.
This dual activation by DVs is a critical factor in the pathobiology of severe malaria.
The DV represents a previously unrecognized determinant of Plasmodium falciparum pathogenicity.
Dextran sulfate demonstrates potential as a therapeutic agent by inhibiting DV-mediated immune activation.