Abstract
Salmonella is a facultative intracellular Gram-negative bacterium, responsible for a wide range of food- and water-borne diseases ranging from gastroenteritis to typhoid fever depending on hosts and serotypes. Salmonella thus represents a major threat to public health. A key step in Salmonella pathogenesis is the invasion of phagocytic and non-phagocytic host cells. To trigger its own internalization into non-phagocytic cells, Salmonella has developed different mechanisms, involving several invasion factors. For decades, it was accepted that Salmonella could only enter cells through a type three secretion system, called T3SS-1. Recent research has shown that this bacterium expresses outer membrane proteins, such as the Rck protein, which is able to induce Salmonella entry mechanism. Rck mimics natural host cell ligands and triggers engulfment of the bacterium by interacting with the epidermal growth factor receptor. Salmonella is thus able to use multiple entry pathways during the Salmonella infection process. However, it is unclear how and when Salmonella exploits the T3SS-1 and Rck entry mechanisms. As a series of reviews have focused on the T3SS-1, this review aims to describe the current knowledge and the limitations of our understanding of the Rck outer membrane protein. The regulatory cascade which controls Rck expression and the molecular mechanisms underlying Rck-mediated invasion into cells are summarized. The potential role of Rck-mediated invasion in Salmonella pathogenesis and the intracellular behavior of the bacteria following a Salmonella Rck-dependent entry are discussed.
Highlights
Salmonella is a Gram-negative, facultative anaerobic and gastrointestinal pathogen belonging to the Enterobacteriaceae family
We demonstrated that varying epidermal growth factor receptor (EGFR) expression on the cell surface altered Salmonella internalization dependent on Resistance to complement killing (Rck)
The mechanism, which has been elucidated the most, requires Type III Secretion System (T3SS)-1 to translocate several bacterial effectors. These effectors interact with host cell partners, inducing profound cytoskeleton and membrane rearrangements, which lead to the bacterium being internalized in an early Salmonella-containing vacuole (SCV) (30 min following internalization), which matures to an intermediate state by acquiring macropinocytic and endocytic components
Summary
Salmonella is a Gram-negative, facultative anaerobic and gastrointestinal pathogen belonging to the Enterobacteriaceae family. Recent data have shown that, even in the absence of the T3SS-1, Salmonella remains able to invade epithelial and fibroblastic cell lines and to enter into 3-D intestinal epithelial cells (Aiastui et al, 2010; Radtke et al, 2010; Rosselin et al, 2011), indicating the existence of other invasion factors. These results are consistent with the fact that a Salmonella strain lacking SPI-1 was isolated from a human food-borne disease outbreak in China (Hu et al, 2008). The aspects of Salmonella invasion mechanisms, which are not covered in our review, are well described in the review of Hume et al (2017)
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