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Evaluation of Extracellular Vesicle Function During Malaria Infection
13:45

Evaluation of Extracellular Vesicle Function During Malaria Infection

Published on: February 14, 2018

Vacuolar uptake of host components, and a role for cholesterol and sphingomyelin in malarial infection

S Lauer1, J VanWye, T Harrison

  • 1Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.

The EMBO Journal
|July 19, 2000
PubMed

Insights

The malaria parasite Plasmodium falciparum internalizes host cell membrane proteins, including Duffy, into its vacuole. This process, regulated by specific lipids, offers new insights into parasitic infection mechanisms.

Area of Science:

  • Cell Biology
  • Parasitology
  • Molecular Biology

Background:

  • Erythrocytes (red blood cells) are infected by Plasmodium falciparum despite lacking endocytosis.
  • Host cell membrane proteins associated with detergent-resistant membranes (DRMs) are implicated in parasite invasion.

Purpose of the Study:

  • To investigate the internalization mechanisms of host cell proteins by Plasmodium falciparum.
  • To identify the host proteins and parasite components within the vacuolar compartment.

Main Methods:

  • Analysis of host proteins associated with detergent-resistant membranes (DRMs) in infected erythrocytes.
  • Detection of internalized host proteins and parasite proteins within the vacuolar membrane.

Main Results:

  • Plasmodium falciparum internalizes Duffy protein and other DRM-associated proteins into its vacuole.
  • Vacuolar parasites contain detergent-resistant membranes (DRMs) with internalized host proteins and a parasite transmembrane protein.
  • Internalization rate of Duffy protein is comparable to a glycosylphosphatidylinositol (GPI)-anchored protein.

Conclusions:

  • Integral membrane proteins can be internalized into the Plasmodium falciparum vacuole.
  • Vacuolar DRMs are present and play a role in host protein uptake and vacuole maintenance.
  • Lipids like sphingomyelin and cholesterol regulate host protein internalization and parasite vacuole stability, impacting pathogenesis.

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