Beschreibung:
<jats:title>Summary</jats:title><jats:p> <jats:italic>Salmonella enterica</jats:italic> serovar Typhimurium can enter non‐phagocytic cells, such as intestinal epithelial cells, by virtue of a Type Three Secretion System (TTSS) encoded in the <jats:italic>Salmonella</jats:italic> Pathogenicity Island 1 (SPI‐1), which translocates bacterial effector molecules into the host cell. <jats:italic>Salmonella</jats:italic> 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 <jats:italic>S.</jats:italic> Typhimurium strain lacking a key component of its TTSS‐1 (ΔInvC) leading to defective translocation of SPI‐1‐encoded effectors. Whereas this mutant <jats:italic>Salmonella</jats:italic> strain was impaired for invasion of non‐phagocytic cells, it was taken up by DCs at a significantly higher rate than wild‐type <jats:italic>Salmonella</jats:italic>. Similar to wild‐type <jats:italic>Salmonella</jats:italic>, the ΔInvC mutant strain retained the capacity to avoid antigen presentation to T cells. However, mice infected with the ΔInvC 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.</jats:p>