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Updated: May 1, 2026
Selection of Plasmodium falciparum Parasites for Cytoadhesion to Human Brain Endothelial Cells
Published on: January 3, 2012
P. falciparum isolate-specific distinct patterns of induced apoptosis in pulmonary and brain endothelial cells
Nadine N'Dilimabaka1, Zacharie Taoufiq1, Sergine Zougbédé1
1Université Pierre et Marie Curie-Paris 6, UMRS 945, Paris, France; Institut National de la Santé et de la Recherche Médicale, UMRS 945, Paris, France.
Abstract:
The factors implicated in the transition from uncomplicated to severe clinical malaria such as pulmonary oedema and cerebral malaria remain unclear. It is known that alterations in vascular integrity due to endothelial cell (EC) activation and death occur during severe malaria. In this study, we assessed the ability of different P. falciparum clinical isolates to induce apoptosis in ECs derived from human lung and brain. We observed that induction of EC apoptosis was sensitive to the environmental pH and required direct contact between the parasite and the cell, though it was not correlated to the ability of the parasite to cytoadhere. Moreover, the extent of induced apoptosis in the two EC types varied with the isolate. Analysis of parasite genes transcript led us to propose that the activation of different pathways, such as Plasmodium apoptosis-linked pathogenicity factors (PALPF), PALPF-2, PALPF-5 and PF11_0521, could be implied in EC death. These observations provide an experimental framework to decipher the molecular mechanism implicated in the genesis of severe malaria.
Insights
Severe malaria involves endothelial cell (EC) death, but underlying factors are unclear. This study reveals Plasmodium falciparum isolates induce EC apoptosis via direct contact and specific parasite factors, offering insights into severe malaria pathogenesis.
Area of Science:
- Malariology
- Cell Biology
- Pathogenesis
Background:
- Severe malaria, including pulmonary edema and cerebral malaria, arises from unclear factors.
- Endothelial cell (EC) activation and death disrupt vascular integrity during severe malaria.
Purpose of the Study:
- To investigate the capacity of Plasmodium falciparum (P. falciparum) clinical isolates to induce apoptosis in human lung and brain ECs.
- To identify parasite-derived factors and conditions influencing EC apoptosis in malaria.
Main Methods:
- Assessed P. falciparum clinical isolates' ability to induce apoptosis in human lung and brain ECs.
- Examined the influence of environmental pH and direct parasite-EC contact on apoptosis.
- Analyzed parasite gene transcripts, including Plasmodium apoptosis-linked pathogenicity factors (PALPF).
Main Results:
- EC apoptosis induction was pH-sensitive and required direct parasite-EC contact, independent of cytoadherence.
- The degree of EC apoptosis varied among different P. falciparum isolates and between lung and brain ECs.
- Specific parasite factors like PALPF, PALPF-2, PALPF-5, and PF11_0521 were implicated in EC death.
Conclusions:
- P. falciparum isolates differentially induce EC apoptosis, contributing to severe malaria pathogenesis.
- Direct contact and specific parasite factors, not cytoadherence, are key in EC apoptosis.
- Understanding these mechanisms provides a framework for deciphering severe malaria development.
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