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Background   Salmonella enterica  serovar Typhimurium is a major foodborne pathogen worldwide.  S.  Typhimurium encodes type III secretion systems via  Salmonella  pathogenicity islands (SPI), producing the major effector proteins of virulence. Previously, we identified two genes of  Salmonella  pyruvate metabolism that were up-regulated during chicken cell infection: pyruvate formate lyase I ( pflB ) and bifunctional acetaldehyde-CoA/alcohol dehydrogenase ( adhE ). We were therefore interested in examining the role these genes may play in the transmission of  Salmonella  to humans.    Methods  Mutant strains of  Salmonella  with single gene deletions for  pflB  and  adhE  were created. Invasion and growth in human HCT-8 intestinal epithelial cells and THP-1 macrophages was examined. Quantitative PCR was performed on 19 SPI-1 genes.    Results  In HCT-8 cells, both mutant strains had significantly higher intracellular counts than the wild-type from 4 to 48 h post-infection. Various SPI-1 genes in the mutants were up-regulated over the wild-type as early as 1 h and lasting until 24 h post-infection. In THP-1 cells, no significant difference in internal  Salmonella  counts was observed; however, SPI-1 genes were largely down-regulated in the mutants during the time-course of infection. We also found five SPI-1 genes -  hilA ,  hilC hilD ,  sicP  and  rtsA  - which were up-regulated in at least one of the mutant strains in log-phase broth cultures alone. We have therefore identified a set of SPI-1 virulence genes whose regulation is effected by the central metabolism of  Salmonella .

Deletions in the pyruvate pathway of Salmonella Typhimurium alter SPI1-mediated gene expression and infectivity