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Microvesicles released from Giardia intestinalis disturb host-pathogen response in vitro
Ingrid Evans-Osses1, Andres Mojoli1, Marta Monguió-Tortajada2
1Fundacao Oswaldo Cruz-Instituto Oswaldo Cruz, Av. Brasil 4365, Manguinhos, Rio de Janeiro, Brazil.
European Journal of Cell Biology
|February 26, 2017
Summary
Microvesicles (MVs) released by Giardia intestinalis trophozoites enhance parasite attachment to host cells and activate human dendritic cells, contributing to giardiasis pathogenesis. Understanding MV biogenesis is crucial for disease control.
Area of Science:
- Parasitology
- Cell Biology
- Immunology
Background:
- Giardia intestinalis (G.I.) causes giardiasis, a global diarrheal disease.
- G.I. has a life cycle involving cyst and trophozoite stages.
- Microvesicles (MVs) are released by eukaryotic cells and observed in G.I. life cycle.
Purpose of the Study:
- Investigate the role of G.I. microvesicles in giardiasis pathogenesis.
- Determine how MVs influence G.I. trophozoite interaction with host cells.
- Assess the impact of G.I. MVs on human immune cells.
Main Methods:
- Observation of MV release during G.I. life cycle.
- Assessing MV effects on G.I. trophozoite attachment to Caco-2 cells.
- Analyzing MV interaction with human immature dendritic cells.
- Investigating the role of lipid rafts in MV biogenesis and function.
- Proteomic analysis of G.I. MVs.
Main Results:
- MVs from log-phase G.I. trophozoites increased trophozoite attachment to Caco-2 cells.
- G.I. MVs were captured by human immature dendritic cells, enhancing their activation and allostimulation.
- Lipid rafts are involved in MV biogenesis and attachment to Caco-2 cells.
- Proteomic analysis revealed minor protein differences between MV types.
Conclusions:
- G.I. MVs play a significant role in giardiasis pathogenesis.
- MVs contribute to G.I. trophozoite adhesion and modulate host immune responses.
- Understanding G.I. MV biogenesis and content is vital for developing therapeutic strategies.
Keywords:
DiarrhoeaExtracellular vesiclesGiardia intestinalisInnate immunityMicrovesiclesParasite-host cell interactions
