| First Author | Bueno SM | Year | 2010 |
| Journal | Immunology | Volume | 130 |
| Issue | 2 | Pages | 273-87 |
| PubMed ID | 20201987 | Mgi Jnum | J:166411 |
| Mgi Id | MGI:4844245 | Doi | 10.1111/j.1365-2567.2009.03233.x |
| Citation | Bueno SM, et al. (2010) Salmonella pathogenicity island 1 differentially modulates bacterial entry to dendritic and non-phagocytic cells. Immunology 130(2):273-87 |
| abstractText | Salmonella enterica serovar Typhimurium can enter non-phagocytic cells, such as intestinal epithelial cells, by virtue of a Type Three Secretion System (TTSS) encoded in the Salmonella Pathogenicity Island 1 (SPI-1), which translocates bacterial effector molecules into the host cell. Salmonella can also be taken up by dendritic cells (DCs). Although the role of SPI-1 in non-phagocytic cell invasion is well established, its contribution to invasion of phagocytic cells has not been evaluated. Here, we have tested the invasive capacity of a S. Typhimurium strain lacking a key component of its TTSS-1 (DeltaInvC) leading to defective translocation of SPI-1-encoded effectors. Whereas this mutant Salmonella strain was impaired for invasion of non-phagocytic cells, it was taken up by DCs at a significantly higher rate than wild-type Salmonella. Similar to wild-type Salmonella, the DeltaInvC mutant strain retained the capacity to avoid antigen presentation to T cells. However, mice infected with the DeltaInvC mutant strain showed higher survival rate and reduced organ colonization. Our data suggest that, besides promoting phagocytosis by non-phagocytic cells, SPI-1 modulates the number of bacteria that enters DCs. The SPI-1 could be considered not only as an inducer of epithelial cell invasion but as a controller of DC entry. |
