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.

Frontiers in Microbiology
|January 24, 2022
PubMed

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.