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Background    Salmonella  pathogenicity island (SPI)-13 is conserved in many serovars of  S. enterica , including  S . Enteritidis,  S . Typhimurium and  S . Gallinarum. However, it is absent in typhoid serovars such as  S . Typhi and Paratyphi A, which carry SPI-8 at the same genomic location. Because the interaction with macrophages is a critical step in  Salmonella  pathogenicity, in this study we investigated the role played by SPI-13 and SPI-8 in the interaction of  S.  Enteritidis and  S.  Typhi with cultured murine (RAW264.7) and human (THP-1) macrophages.    Results   Our results showed that SPI-13 was required for internalization of  S.  Enteritidis in murine but not human macrophages. On the other hand, SPI-8 was not required for the interaction of  S.  Typhi with human or murine macrophages. Of note, the presence of an intact copy of SPI-13 in a  S . Typhi mutant carrying a deletion of SPI-8 did not improve its ability to be internalized by, or survive in human or murine macrophages.    Conclusions  Altogether, our results point out to different roles for SPI-13 and SPI-8 during  Salmonella  infection. While SPI-13 contributes to the interaction of  S . Enteritidis with murine macrophages, SPI-8 is not required in the interaction of  S.  Typhi with murine or human macrophages. We hypothesized that typhoid serovars have lost SPI-13 and maintained SPI-8 to improve their fitness during another phase of human infection.    Electronic supplementary material  The online version of this article (doi:10.1186/s40659-017-0109-8) contains supplementary material, which is available to authorized users.

biological research

Differential roles for pathogenicity islands SPI-13 and SPI-8 in the interaction of Salmonella Enteritidis and Salmonella Typhi with murine and human macrophages