Aims: Salmonella enterica serovar Typhimurium is capable of adopting a filamentous phenotype in response to damage. How this adaptive response affects bacterial virulence is unclear. We have examined the hypothesis that filamentation affects the ability of Salmonella to infect host cells.
Methods and Results: Expression of the cell division inhibitor SulA in Salm. Typhimurium SL1344 from an arabinose-inducible plasmid resulted in filamentation. We examined expression of the type 3 secretion system (T3SS) encoded by Salmonella pathogenicity island 1 (SPI-1) using SL1344 expressing a chromosomal PprgH-gfp reporter. Single cell analysis of SulA-induced SL1344 PprgH-gfp revealed a relationship between increasing cell length and decreasing propensity for prgH expression, but there was no evidence of a significant change in prgH expression evident at the whole population level. Filamentous Salm. Typhimurium were capable of initiating membrane ruffling on MDCK epithelial cells, but only nonfilamentous bacteria (<6 μm) invade.
Conclusions: Induction of SulA expression in Salmonella inhibits septation. Increasing filament length is associated with down-regulation of SPI-1 gene expression, but a significant proportion of filaments retain the ability to produce SPI-1 T3SS and induce membrane ruffles on epithelia. Despite an active SPI-1 T3SS, filamentous Salmonella are unable to invade epithelial cells.
Significance and Impact of the Study: Our findings that filamentous Salmonella can express an invasive phenotype but fail to invade cells suggest that their presence in food does not constitute an immediate risk of infection until septation occurs. The described SulA expression model provides a convenient model for studying the impact of filamentation in the absence of additional stresses.