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Lipid-Rich Extracellular Vesicles in<em> Leishmania (L.) amazonensis</em>: Ultrastructural Evidence and Functional Implications for Parasite–Host Interaction
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Extracellular vesicles released by Leishmania spp. (LEVs) are increasingly recognized as key mediators of parasite communication and host immune modulation. Lipids, although central to LEV biogenesis and function, remain understudied in the context of Leishmania pathogenicity. Here, we investigated the presence and distribution of lipid-rich structures in Leishmania (L.) amazonensis promastigotes and intracellular amastigotes using transmission electron microscopy (TEM), scanning electron microscopy (SEM), and fluorescence microscopy with Bodipy staining. Promastigotes at the stationary phase exhibited abundant vesicle accumulation in the flagellar pocket, Golgi-associated autophagic structures, and lipid body–like inclusions. Infected BALB/c peritoneal macrophages contained amastigotes within parasitophorous vacuoles, also displaying lipid-rich compartments. Bodipy staining confirmed the presence of neutral lipid bodies in promastigotes, supporting their involvement in LEV formation. These findings suggest that lipid-enriched LEVs contribute to membrane remodeling, intracellular survival, and host cell modulation. Our study provides experimental evidence supporting lipid-centered mechanisms in Leishmania LEV biology and highlights potential targets for therapeutic intervention.
Title: Lipid-Rich Extracellular Vesicles in<em> Leishmania (L.) amazonensis</em>: Ultrastructural Evidence and Functional Implications for Parasite–Host Interaction
Description:
Extracellular vesicles released by Leishmania spp.
(LEVs) are increasingly recognized as key mediators of parasite communication and host immune modulation.
Lipids, although central to LEV biogenesis and function, remain understudied in the context of Leishmania pathogenicity.
Here, we investigated the presence and distribution of lipid-rich structures in Leishmania (L.
) amazonensis promastigotes and intracellular amastigotes using transmission electron microscopy (TEM), scanning electron microscopy (SEM), and fluorescence microscopy with Bodipy staining.
Promastigotes at the stationary phase exhibited abundant vesicle accumulation in the flagellar pocket, Golgi-associated autophagic structures, and lipid body–like inclusions.
Infected BALB/c peritoneal macrophages contained amastigotes within parasitophorous vacuoles, also displaying lipid-rich compartments.
Bodipy staining confirmed the presence of neutral lipid bodies in promastigotes, supporting their involvement in LEV formation.
These findings suggest that lipid-enriched LEVs contribute to membrane remodeling, intracellular survival, and host cell modulation.
Our study provides experimental evidence supporting lipid-centered mechanisms in Leishmania LEV biology and highlights potential targets for therapeutic intervention.
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