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Selection of Plasmodium falciparum Parasites for Cytoadhesion to Human Brain Endothelial Cells
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Cytoadhesion of Plasmodium falciparum-Infected Red Blood Cells Changes the Expression of Cytokine-, Histone- and

Johannes Allweier1,2, Michael Bartels1, Hanifeh Torabi1

  • 1Research Group Host-Parasite Interaction, Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany.

Molecular Microbiology
|December 4, 2024
PubMed

Insights

Malaria-infected red blood cells (iRBCs) trigger endothelial cell responses, activating immune and angiogenic pathways. Fever exacerbates these effects, highlighting iRBCs

Area of Science:

  • Immunology and Infectious Diseases
  • Vascular Biology and Endothelial Function
  • Genomics and Transcriptomics

Background:

  • Malaria, caused by Plasmodium falciparum, leads to severe infections and mortality.
  • Infected red blood cells (iRBCs) adhere to endothelial cells (ECs), causing vascular dysfunction and inflammation.
  • Understanding the endothelial transcriptional response to iRBCs is crucial for malaria pathogenesis research.

Purpose of the Study:

  • To investigate the effects of iRBC binding on endothelial cells (ECs) at normal and fever temperatures.
  • To analyze the transcriptional changes in ECs induced by iRBCs and non-infected RBCs (niRBCs).
  • To identify specific signaling pathways activated in ECs during malaria infection.

Main Methods:

  • Utilized an in vitro model: iRBCIT4var04/HBEC-5i.
  • Compared gene expression profiles of ECs exposed to iRBCs versus niRBCs at 37°C and 40°C.
  • Analyzed transcriptional responses including immune, angiogenic, and interferon signaling pathways.

Main Results:

  • Both niRBCs and fever alone significantly altered EC gene expression.
  • iRBC binding upregulated genes involved in immune response, nucleosome assembly, NF-kappa B signaling, angiogenesis, and interferon signaling.
  • Simulated fever (40°C) further amplified gene expression, particularly for cytokine production and angiogenesis.

Conclusions:

  • iRBCs stimulate ECs, activating immunological pathways and impacting antiviral mechanisms.
  • The interferon-alpha/beta signaling pathway is significantly induced in ECs by iRBCs.
  • Fever intensifies the endothelial response, suggesting a complex interplay between infection and host temperature.
Keywords:
Plasmodium falciparumcytoadhesionendothelial cellsfevermalariatranscriptome

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