Leishmania amazonensis sabotages host cell SUMOylation for intracellular survival

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Updated: Oct 2, 2026

Quantification of Intracellular Growth Inside Macrophages is a Fast and Reliable Method for Assessing the Virulence of Leishmania Parasites
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Quantification of Intracellular Growth Inside Macrophages is a Fast and Reliable Method for Assessing the Virulence of Leishmania Parasites

Published on: March 16, 2018

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Kendi Okuda1, Miriam Maria Silva Costa Franco1, Ari Yasunaga2

  • 1Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, USA.

Iscience
|September 5, 2022
PubMed

Insights

Leishmania parasites sabotage host SUMOylation to boost their growth inside macrophages. This manipulation enhances parasite replication by altering host cell genes and creating a better intracellular niche.

Area of Science:

  • Cell Biology
  • Parasitology
  • Immunology

Background:

  • Leishmania parasites employ sophisticated virulence strategies to infect macrophages, inhibiting host defenses and establishing a replicative niche called the parasitophorous vacuole.
  • Understanding host factors crucial for Leishmania infection is vital for developing targeted therapies.

Purpose of the Study:

  • To identify host factors essential for Leishmania amazonensis infection using a genome-wide RNA interference (RNAi) screen.
  • To investigate the role of SUMOylation in Leishmania infection and its impact on the host cell.

Main Methods:

  • A genome-wide RNAi screen was conducted in Drosophila macrophage-like cells to identify host genes involved in Leishmania amazonensis entry.
  • Subsequent studies in mammalian macrophages analyzed the effects of L. amazonensis infection on SUMOylation and host gene expression.

Main Results:

  • The screen identified 52 conserved genes critical for parasite entry, including components of the SUMOylation pathway.
  • Leishmania amazonensis infection was found to inhibit SUMOylation in macrophages, promoting parasitophorous vacuole growth and parasite proliferation.
  • This inhibition modulated host genes, notably ATP6V0D2, influencing CD36 expression and cholesterol levels.

Conclusions:

  • Leishmania parasites actively disrupt host SUMOylation processes to optimize their intracellular environment.
  • Altering host transcription, particularly affecting ATP6V0D2 and CD36, is a key mechanism by which parasites enhance their replication within macrophages.
Keywords:
ImmunologyParasitology

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