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Host cell death induced by the egress of intracellular Plasmodium parasites

Volker Heussler1, Annika Rennenberg, Rebecca Stanway

  • 1Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany. heussler@bni-hamburg.de

Apoptosis : an International Journal on Programmed Cell Death
|December 17, 2009
PubMed

Insights

Intracellular pathogens like Plasmodium can trigger a unique cell death in host hepatocytes. This parasite-dependent process, crucial for pathogen egress, involves parasitophorous vacuole membrane rupture.

Area of Science:

  • Cell Biology
  • Pathogen-Host Interactions
  • Parasitology

Background:

  • Intracellular pathogens inhibit host apoptosis for survival.
  • Pathogen egress from host cells is essential for infection spread.
  • Plasmodium parasites infect various host cells, including erythrocytes and hepatocytes.

Purpose of the Study:

  • To investigate the mechanism of cell death in Plasmodium-infected hepatocytes.
  • To differentiate this cell death from apoptosis and necrosis.
  • To identify key events and molecular players involved in parasite-induced hepatocyte death.

Main Methods:

  • Observation of Plasmodium-infected hepatocytes.
  • Analysis of host cell death morphology and markers.
  • Investigation of parasitophorous vacuole membrane integrity.
  • Assessment of cysteine protease activity.

Main Results:

  • Plasmodium-infected hepatocytes undergo an ordered, parasite-dependent cell death.
  • This cell death is distinct from apoptosis and necrosis.
  • Parasitophorous vacuole membrane rupture is a critical, irreversible event.
  • Cysteine protease activation, of either parasite or host origin, drives PVM disruption and cell death.

Conclusions:

  • Plasmodium-induced hepatocyte death is a regulated process essential for parasite egress.
  • Parasitophorous vacuole membrane rupture, mediated by cysteine proteases, is the key event.
  • The specific proteases involved depend on the Plasmodium life cycle stage and host cell type.

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