Abstract
To establish an infection, Salmonella has to interact with eukaryotic cells. Invasion of non-phagocytic cells (i.e., epithelial, fibroblast and endothelial cells) involves either a trigger or a zipper mechanism mediated by the T3SS-1 or the invasin Rck, respectively. Another outer membrane protein, PagN, was also implicated in the invasion. However, other unknown invasion factors have been previously suggested. Our goal was to evaluate the invasion capability of a Salmonella Typhimurium strain invalidated for the three known invasion factors. Non-phagocytic cell lines of several animal origins were tested in a gentamicin protection assay. In most cells, we observed a drastic decrease in the invasion rate between the wild-type and the triple mutant. However, in five cell lines, the triple mutant invaded cells at a similarly high level to the wild-type, suggesting the existence of unidentified invasion factors. For the wild-type and the triple mutant, scanning-electron microscopy, confocal imaging and use of biochemical inhibitors confirmed their cellular uptake and showed a zipper-like mechanism of internalization involving both clathrin- and non-clathrin-dependent pathways. Despite a functional T3SS-1, the wild-type bacteria seemed to use the same entry route as the mutant in our cell model. All together, these results demonstrate the existence of unknown Salmonella invasion factors, which require further characterization.
Highlights
No relation could be established according to the origin of the cells, as these results were obtained with four epithelial cell lines of different origins (Caco-2, Ma104, AML-12, and IPEC-1) and one endothelial cell line
As extensive or low cell rearrangement leads to trigger- or a zipper-like entry mechanism, respectively and as confocal imaging did not enable identification of the process involved, we examined the morphological alterations occurring in AML-12 cells during bacterial uptake under a scanning-electron microscope (Figure 4)
Salmonella Typhimurium invasion, and the role of the T3SS-1, has been extensively characterized in cultured epithelial cells. This invasion process involves a subset of T3SS-1 effectors (SipA, SipC, SopB, SopE, SopE2) acting in concert to induce massive localized rearrangements of actin at the plasma membrane level, and to activate signaling pathways resulting in membrane ruffling and macropinocytosis at the site of Salmonella-epithelial cell contact (Mcghie et al, 2009; Aiastui et al, 2010; Dunn and Valdivia, 2010)
Summary
Typhimurium) is one of the broad host range serotypes incriminated in food-borne diseases in industrial countries. The bacteria are commonly found in the intestinal tracts of healthy birds and mammals, resulting in a spectrum of outcomes ranging from severe systemic disease to asymptomatic carriage (Velge et al, 2012). The Typhimurium serovar causes enterocolitis, and infected animals can succumb to dehydration. It causes systemic disease and diarrhea, whereas older chickens are asymptomatic carriers. It could be responsible for a typhoid fever like disease in susceptible mouse strains (Santos et al, 2001)
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