Actin-gated intracellular growth and resurgence of uropathogenic Escherichia coli.

摘要: Strains of uropathogenic Escherichia coli (UPEC) can invade terminally differentiated superficial bladder epithelial cells and subsequently multiply, forming large biofilm-like inclusions referred to as pods. In contrast, within immature UPEC enter a more quiescent state often fail replicate appreciably. As undergo terminal differentiation the actin cytoskeleton is radically diminished, phenomenon that we reasoned could influence intracellular fate UPEC. Here show undifferentiated trafficked into acidic compartments having key features late endosomes lysosomes. These UPEC-containing vacuoles are enmeshed network filaments, disruption which stimulates intravacuolar growth efflux in cell culture-based studies. this vitro model system, release host cytosol further bacterial rapid development pod-like inclusions. inclusions, well those observed using an vivo mouse model, develop association with cytokeratin intermediate filaments may act scaffolding for biofilm formation. Our data suggest aetiological basis recurrent urinary tract infections, linking accompanying redistribution microfilaments resurgence from reservoirs epithelium.