作者: Isabelle Guérin , Chantal de Chastellier
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摘要: Phagosomes containing live virulent mycobacteria undergo fusion with early endosomes, but they are unable to mature normally. Accordingly, do not fuse lysosomes. Although M. avium-containing phagosomes retain and intermingling characteristics of endosomes indefinitely, fusions increasingly restricted as bacteria multiply. In addition, when endocytic tracers, such horseradish peroxidase (HRP), added avium-infected macrophages at 1 or up 15 days after infection, an atypical time course acquisition the tracer by is observed, i.e., a 10 20 min lag, instead immediate typical for (and endosome characteristics). These events coincide marked disorganization actin filament network in macrophages. present study, we have therefore addressed following question: Do filaments play role contents between immature that homotypic endosomes? We examined subsequently internalized marker (HRP) endosome-like preexisting phagosomes, i.e. 2 hour-old either hydrophobic latex particles, avirulent avium, depolymerization cytochalasin D repolymerization jasplakinolide, cases where had been depolymerized (macrophages infected 7 infection). By direct morphological observation electron microscope level kinetic approach, show here delays HRP whereas restores marker. conclude involved disruption this avium cause content these pathogenic mycobacteria.