The parasitophorous vacuole membrane of Encephalitozoon cuniculi lacks host cell membrane proteins immediately after

Verena Fasshauer1, Uwe Gross, Wolfgang Bohne

  • 1Institute of Medical Microbiology, University of Göttingen, Göttingen, Germany.

Eukaryotic Cell
|January 12, 2005
PubMed

Insights

Microsporidia parasites form a unique vacuole during infection. This parasitophorous vacuole (PV) avoids cellular pathways and remains nonfusogenic, even after drug treatment.

Area of Science:

  • Cell Biology
  • Parasitology
  • Microbiology

Background:

  • Microsporidia are obligate intracellular parasites.
  • Encephalitozoon species cause opportunistic infections.
  • The origin and nature of the parasitophorous vacuole (PV) are poorly understood.

Purpose of the Study:

  • To investigate the origin and characteristics of the PV in Encephalitozoon infections.
  • To determine if the PV interacts with host endocytic or endoplasmic reticulum pathways.
  • To assess the effect of anti-parasitic drugs on PV properties.

Main Methods:

  • Colocalization studies using specific cellular markers.
  • Immunofluorescence microscopy to visualize PV and host markers.
  • Treatment with albendazole and fumagillin.

Main Results:

  • The PV was absent from endocytic pathway markers (early endosomal autoantigen 1, transferrin receptor, lysosome-associated membrane protein 1).
  • The PV marker calnexin (endoplasmic reticulum) was also absent.
  • The PV exhibited nonfusogenic characteristics within 1 minute postinfection.
  • Drug treatments with albendazole and fumagillin did not alter the PV's nonfusogenic nature.

Conclusions:

  • The parasitophorous vacuole (PV) in Encephalitozoon infections originates independently of host endocytic and endoplasmic reticulum pathways.
  • The PV rapidly acquires a nonfusogenic state upon infection.
  • This nonfusogenic characteristic is resistant to common anti-microsporidial drugs.

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