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Enteropathogenic Escherichia coli induces Entamoeba histolytica superdiffusion movement on fibronectin by reducing traction forces
Enteropathogenic Escherichia coli induces Entamoeba histolytica superdiffusion movement on fibronectin by reducing traction forces
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Enteropathogenic Escherichia coli induces Entamoeba histolytica superdiffusion movement on fibronectin by reducing traction forces
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Enteropathogenic Escherichia coli induces Entamoeba histolytica superdiffusion movement on fibronectin by reducing traction forces
Enteropathogenic Escherichia coli induces Entamoeba histolytica superdiffusion movement on fibronectin by reducing traction forces

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Enteropathogenic Escherichia coli induces Entamoeba histolytica superdiffusion movement on fibronectin by reducing traction forces
Enteropathogenic Escherichia coli induces Entamoeba histolytica superdiffusion movement on fibronectin by reducing traction forces
Journal Article

Enteropathogenic Escherichia coli induces Entamoeba histolytica superdiffusion movement on fibronectin by reducing traction forces

2025
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Overview
Amebiasis, caused by Entamoeba histolytica , is a global health concern, affecting millions and causing significant mortality, particularly in areas with poor sanitation. Although recent studies have examined E. histolytica ’s interaction with human intestinal microbes, the impact of bacterial presence on the parasite’s motility, mechanical forces, and their potential role in altering invasiveness have not been fully elucidated. In this study, we utilized a micropillar-array system combined with live imaging to investigate the effects of enteropathogenic Escherichia coli on E. histolytica ’s motility characteristics, F-actin spatial localization, and traction force exerted on fibronectin-coated substrates. Our findings indicate that co-incubation with live enteropathogenic E. coli significantly enhances the motility of E. histolytica , as evidenced by superdiffusive movement—characterized by increased directionality and speed—resulting in broader dispersal and more extensive tissue/cell damage. This increased motility is accompanied by a reduction in F-actin-dependent traction forces and podosome-like structures on fibronectin-coated substrates, but with increased F-actin localization in the upper part of the cytoplasm. These findings highlight the role of physical interactions and cellular behaviors in modulating the parasite’s virulence, providing new insights into the mechanistic basis of its pathogenicity.

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