Abstract

A common strategy among intracellular bacterial pathogens is to enter into a vacuolar environment upon host cell invasion. One such pathogen, Salmonella enterica, resides within the Salmonella-containing vacuole (SCV) inside epithelial cells and macrophages. Salmonella hijacks the host endosomal system to establish this unique intracellular replicative niche, forming a highly complex and dynamic network of Salmonella-induced filaments (SIFs). SIFs radiate outwards from the SCV upon onset of bacterial replication. SIF biogenesis is dependent on the activity of bacterial effector proteins secreted by the Salmonella-pathogenicity island-2 (SPI-2) encoded type III secretion system. While the presence of SIFs has been known for almost 25 years, their precise role during infection remains elusive. This review summarizes our current knowledge of SCV maturation and SIF biogenesis, and recent advances in our understanding of the role of SIFs inside cells.

Highlights

  • Salmonella enterica serovars are Gram-negative bacterial pathogens capable of causing enteric disease in all vertebrates

  • This review focuses on intravacuolar Salmonella, but a small portion of Salmonella escape the Salmonella-containing vacuole (SCV) and enter a hyper-replicative state within the cytosol of epithelial cells (Knodler et al, 2010; Malik-Kale et al, 2012; Yu et al, 2014; Santos et al, 2015)

  • Krieger et al propose a model of Salmonella-induced filaments (SIFs) biogenesis wherein SPI2-T3SS-secreted effectors, in particular SifA, recruit and fuse host membrane vesicles to the SCV providing components for tubule extension

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Summary

Introduction

Salmonella enterica serovars are Gram-negative bacterial pathogens capable of causing enteric disease in all vertebrates. Studies primarily in HeLa cells have revealed that formation of the early SCV is dependent on SPI1-T3SS-secreted effectors (red arrow) and occurs within 15 min post-invasion (p.i.). Extensive vacuolation of LAMP1+ vesicles is observed in uninfected host cells transfected with SifA (Brumell et al, 2001a) suggesting that SifA alone is sufficient to induce endosomal tubulation resembling SIF-like structures.

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