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Updated: May 17, 2026

Investigating the Phagocytosis of Leishmania using Confocal Microscopy
Published on: July 29, 2021
Leishmania promastigotes: building a safe niche within macrophages
Neda Moradin1, Albert Descoteaux
1INRS - Institut Armand-Frappier and Center for Host-Parasite Interactions Laval, QC, Canada.
Abstract:
Upon their internalization by macrophages, Leishmania promastigotes inhibit phagolysosome biogenesis. The main factor responsible for this inhibition is the promastigote surface glycolipid lipophosphoglycan (LPG). This glycolipid has a profound impact on the phagosome, causing periphagosomal accumulation of F-actin and disruption of phagosomal lipid microdomains. Functionally, this LPG-mediated inhibition of phagosome maturation is characterized by an impaired assembly of the NADPH oxidase and the exclusion of the vesicular proton-ATPase from phagosomes. In this chapter, we review the current knowledge concerning the nature of the intra-macrophage compartment in which Leishmania donovani promastigotes establish infection. We also describe how LPG enables this parasite to remodel the parasitophorous vacuole.
Insights
Leishmania donovani parasites, specifically their lipophosphoglycan (LPG), prevent macrophage phagolysosome maturation. This process involves disrupting the phagosome and blocking key enzymes necessary for parasite destruction.
Area of Science:
- Immunology
- Cell Biology
- Parasitology
Background:
- Leishmania donovani infects macrophages, establishing a niche within the host cell.
- Phagolysosome biogenesis is crucial for clearing internalized pathogens.
Purpose of the Study:
- To review the mechanisms by which Leishmania donovani promastigotes inhibit phagolysosome maturation.
- To elucidate the role of lipophosphoglycan (LPG) in remodeling the parasitophorous vacuole.
Main Methods:
- Review of existing literature on Leishmania-macrophage interactions.
- Analysis of the molecular and cellular effects of LPG on phagosomes.
Main Results:
- Lipophosphoglycan (LPG) is the primary factor inhibiting phagolysosome biogenesis.
- LPG causes F-actin accumulation and disrupts lipid microdomains within the phagosome.
- LPG impairs NADPH oxidase assembly and excludes proton-ATPase from the phagosome.
Conclusions:
- Leishmania donovani utilizes LPG to actively remodel the phagosome into a survival vacuole.
- Understanding LPG's function is key to developing strategies against Leishmania infections.
