Association of Plasmodium falciparum with human endothelial cells in vitro

Christopher Utter, Adelfa E. Serrano, John W. Glod, Michael J Leibowitz

Research output: Contribution to journalArticlepeer-review

2 Scopus citations


Endothelial abnormalities play a critical role in the pathogenesis of malaria caused by the human pathogen, Plasmodium falciparum. In serious infections and especially in cerebral malaria, red blood cells infected with the parasite are sequestered in small venules in various organs, resulting in endothelial activation and vascular occlusion, which are believed to be largely responsible for the morbidity and mortality caused by this infection, especially in children. We demonstrate that after incubation with infected red blood cells (iRBCs†), cultured human umbilical vein endothelial cells (HUVECs) contain parasite protein, genomic DNA, and RNA, as well as intracellular vacuoles with apparent parasitederived material, but not engulfed or adherent iRBCs. The association of this material with the HUVECs is observed over 96 hours after removal of iRBCs. This phenomenon may occur in endothelial cells in vivo by the process of trogocytosis, in which transfer of material between cells depends on direct cell contact. This process may contribute to the endothelial activation and disruption involved in the pathogenesis of cerebral malaria.

Original languageEnglish (US)
Pages (from-to)183-193
Number of pages11
JournalYale Journal of Biology and Medicine
Issue number2
StatePublished - Jun 1 2017


  • Endothelial cells
  • Malaria
  • Plasmodium falciparum
  • Trogocytosis

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)


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