Related Experiment Video
Updated: Oct 5, 2025

In Vivo Assessment of Rodent Plasmodium Parasitemia and Merozoite Invasion by Flow Cytometry
Published on: April 5, 2015
Cytoadherence Properties of Plasmodium knowlesi-Infected Erythrocytes
Wenn-Chyau Lee1,2, Shahhaziq Shahari1, Samantha Yee Teng Nguee2,3
1Department of Parasitology, Faculty of Medicine, Universiti Malaya, Kuala Lumpur, Malaysia.
Abstract:
Plasmodium knowlesi is responsible for zoonotic malaria infections that are potentially fatal. While the severe pathology of falciparum malaria is associated with cytoadherence phenomena by Plasmodium falciparum-infected erythrocytes (IRBC), information regarding cytoadherence properties of P. knowlesi-IRBC remained scarce. Here, we characterized the cytoadherence properties of RBC infected with the laboratory-adapted P. knowlesi A1-H.1 strain. We found that late-stage IRBC formed rosettes in a human serum-dependent manner, and rosettes hampered IRBC phagocytosis. IRBC did not adhere much to unexposed (unstimulated) human endothelial cell lines derived from the brain (hCMEC/D3), lungs (HPMEC), and kidneys (HRGEC). However, after being "primed" with P. knowlesi culture supernatant, the IRBC-endothelial cytoadherence rate increased in HPMEC and HRGEC, but not in hCMEC/D3 cells. Both endothelial cytoadherence and rosetting phenomena were abrogated by treatment of P. knowlesi-IRBC with trypsin. We also found that different receptors were involved in IRBC cytoadherence to different types of endothelial cells. Although some of the host receptors were shared by both P. falciparum- and P. knowlesi-IRBC, the availability of glycoconjugates on the receptors might influence the capacity of P. knowlesi-IRBC to cytoadhere to these receptors.
Insights
Plasmodium knowlesi-infected red blood cells form rosettes, hindering phagocytosis. These cells adhere to primed endothelial cells, with different receptors involved, unlike Plasmodium falciparum infections.
Area of Science:
- Malariology
- Infectious Diseases
- Cell Biology
Background:
- Plasmodium knowlesi causes severe zoonotic malaria.
- Cytoadherence of P. knowlesi-infected erythrocytes (IRBC) is poorly understood.
- P. falciparum cytoadherence is linked to severe malaria pathology.
Purpose of the Study:
- Characterize cytoadherence properties of P. knowlesi IRBC.
- Investigate rosetting and endothelial cell adhesion.
- Identify involved host receptors and compare with P. falciparum.
Main Methods:
- Used laboratory-adapted P. knowlesi A1-H.1 strain.
- Assessed rosetting and phagocytosis inhibition.
- Tested IRBC adherence to unstimulated and primed endothelial cell lines (hCMEC/D3, HPMEC, HRGEC).
- Used trypsin treatment to abrogate adhesion and rosetting.
Main Results:
- Late-stage P. knowlesi IRBC formed rosettes in a serum-dependent manner, inhibiting phagocytosis.
- IRBC showed low adherence to unstimulated endothelial cells.
- Priming with P. knowlesi supernatant increased IRBC adherence to HPMEC and HRGEC, but not hCMEC/D3.
- Trypsin treatment abolished rosetting and endothelial cytoadherence.
- Different receptors mediated adherence to various endothelial cells.
- Shared receptors with P. falciparum IRBC, but glycoconjugate availability differed.
Conclusions:
- P. knowlesi IRBC exhibit cytoadherence and rosetting, potentially contributing to severe malaria.
- Adherence mechanisms differ from P. falciparum, involving specific receptor-glycoconjugate interactions.
- Further research is needed to fully elucidate P. knowlesi pathogenesis.
More Related Videos
Related Concept Videos
Diversity of Protists II
Symbiosis

