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Impaired cytoadherence of Plasmodium falciparum-infected erythrocytes containing sickle hemoglobin

Rushina Cholera1, Nathaniel J Brittain, Mark R Gillrie

  • 1Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

Proceedings of the National Academy of Sciences of the United States of America
|January 15, 2008
PubMed

Insights

Sickle trait (HbAS) protects children against severe malaria by reducing how infected red blood cells stick to blood vessels. This mechanism involves altered parasite proteins on the red blood cell surface.

Area of Science:

  • Genetics
  • Immunology
  • Infectious Diseases

Background:

  • Sickle trait (HbAS) offers protection against malaria in African populations.
  • Individuals with sickle trait exhibit lower parasite densities and reduced malaria severity.
  • The precise mechanisms underlying this protective effect are not fully understood.

Purpose of the Study:

  • To investigate the cytoadherence properties of Plasmodium falciparum-infected erythrocytes in sickle trait individuals.
  • To elucidate the role of erythrocyte binding in malaria pathogenesis and protection.

Main Methods:

  • Comparison of cytoadherence of parasitized sickle trait (AS) and normal (AA) erythrocytes to endothelial cells and monocytes.
  • Analysis of the display of Plasmodium falciparum erythrocyte membrane protein-1 (PfEMP-1) on infected erythrocytes.

Main Results:

  • Parasitized AS erythrocytes exhibit significantly reduced binding to microvascular endothelial cells and monocytes compared to AA erythrocytes.
  • This reduced binding correlates with altered expression of PfEMP-1, a key parasite adhesion molecule.
  • The findings suggest a mechanism of malaria protection linked to impaired cytoadherence.

Conclusions:

  • Sickle trait confers malaria protection by reducing the cytoadherence of infected erythrocytes.
  • Altered PfEMP-1 display on the erythrocyte surface is a key factor in this protective mechanism.
  • Coinherited factors and acquired immunity may further modulate malaria protection in sickle trait individuals.

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