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ICAM-1 can play a major role in mediating P. falciparum adhesion to endothelium under flow

Carolyn Gray1, Christopher McCormick, Gareth Turner

  • 1Molecular Biochemistry and Parasitology, Liverpool School of Tropical Medicine, Pembroke Place, Liverpool L3 5QA, UK.

Molecular and Biochemical Parasitology
|May 14, 2003
PubMed

Insights

Intercellular Adhesion Molecule-1 (ICAM-1) is critical for Plasmodium falciparum adhesion to endothelial cells under flow. While CD36 also contributes, ICAM-1 blockade severely impairs parasite binding, highlighting its essential role.

Area of Science:

  • Immunology
  • Parasitology
  • Cell Biology

Background:

  • Plasmodium falciparum (P. falciparum) infection causes malaria.
  • P. falciparum-infected red blood cells (IRBCs) adhere to endothelial cells.
  • Adhesion is mediated by parasite ligands binding to host cell receptors like ICAM-1 and CD36.

Purpose of the Study:

  • To investigate the cooperative roles of ICAM-1 and CD36 in P. falciparum adhesion to endothelial cells under flow.
  • To determine the critical adhesion molecule for P. falciparum binding to activated endothelium.

Main Methods:

  • Utilized three laboratory parasite lines and one patient isolate with varying ICAM-1 and CD36 binding avidity.
  • Assessed IRBC adhesion to endothelial cells under flow conditions.
  • Blocked ICAM-1 and CD36 individually to quantify their impact on adhesion.

Main Results:

  • Separate blockade of ICAM-1 and CD36 reduced IRBC adhesion by up to 95% and 50%, respectively.
  • ICAM-1 blockade severely impaired binding under flow conditions, indicating its critical role.
  • Combined ICAM-1 and CD36 synergy mediated the majority (> or =98%) of adhesion once initial binding occurred.

Conclusions:

  • ICAM-1 is essential for P. falciparum adhesion to activated endothelium under flow.
  • Synergy between ICAM-1 and CD36 is crucial for robust IRBC adhesion.
  • Targeting ICAM-1 could be a potential strategy to inhibit P. falciparum cytoadherence.

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