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Updated: May 5, 2026

Selection of Plasmodium falciparum Parasites for Cytoadhesion to Human Brain Endothelial Cells
Published on: January 3, 2012
Plasmodium falciparum adhesion on human brain microvascular endothelial cells involves transmigration-like cup
Ronan Jambou1, Valery Combes, Marie-Jose Jambou
1Vascular Immunology Unit, Department of Pathology and Bosch Institute, Sydney Medical School, The University of Sydney, New South Wales, Australia. rjambou@pasteur.fr
Abstract:
Cerebral malaria, a major cause of death during malaria infection, is characterised by the sequestration of infected red blood cells (IRBC) in brain microvessels. Most of the molecules implicated in the adhesion of IRBC on endothelial cells (EC) are already described; however, the structure of the IRBC/EC junction and the impact of this adhesion on the EC are poorly understood. We analysed this interaction using human brain microvascular EC monolayers co-cultured with IRBC. Our study demonstrates the transfer of material from the IRBC to the brain EC plasma membrane in a trogocytosis-like process, followed by a TNF-enhanced IRBC engulfing process. Upon IRBC/EC binding, parasite antigens are transferred to early endosomes in the EC, in a cytoskeleton-dependent process. This is associated with the opening of the intercellular junctions. The transfer of IRBC antigens can thus transform EC into a target for the immune response and contribute to the profound EC alterations, including peri-vascular oedema, associated with cerebral malaria.
Insights
In cerebral malaria, infected red blood cells transfer material to brain endothelial cells, altering their function and contributing to disease. This interaction opens intercellular junctions, making endothelial cells targets for immune responses.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Cerebral malaria is a lethal complication of malaria, marked by infected red blood cell sequestration in brain microvessels.
- While IRBC adhesion molecules are known, the IRBC/EC junction structure and EC impact remain unclear.
Purpose of the Study:
- To investigate the structural and functional consequences of infected red blood cell (IRBC) and brain endothelial cell (EC) interactions.
- To elucidate the mechanisms underlying EC alterations in cerebral malaria.
Main Methods:
- Co-culture of human brain microvascular EC monolayers with IRBC.
- Analysis of material transfer, antigen uptake, and intercellular junction dynamics.
Main Results:
- Demonstrated a trogocytosis-like transfer of IRBC material to ECs.
- Observed TNF-enhanced IRBC engulfment and parasite antigen transfer to EC endosomes.
- Showed cytoskeleton-dependent antigen transfer and opening of intercellular EC junctions.
Conclusions:
- IRBC antigen transfer transforms ECs into immune targets, contributing to cerebral malaria pathology.
- Adhesion-induced EC alterations, including junction opening and potential edema, are key features of severe malaria.
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