title: Salmonella pathogenicity island 1 differentially modulates bacterial entry to dendritic and non-phagocytic cells.
abstract: 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.
authors.affiliation: Millennium Nucleus on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile. sbueno@bio.puc.cl
authors.forename: Susan M
authors.initials: SM
authors.lastname: Bueno
authors.forename: Aniela
authors.initials: A
authors.lastname: Wozniak
authors.forename: Eduardo D
authors.initials: ED
authors.lastname: Leiva
authors.forename: Sebastián A
authors.initials: SA
authors.lastname: Riquelme
authors.forename: Leandro J
authors.initials: LJ
authors.lastname: Carreño
authors.forename: Wolf-Dietrich
authors.initials: WD
authors.lastname: Hardt
authors.forename: Claudia A
authors.initials: CA
authors.lastname: Riedel
authors.forename: Alexis M
authors.initials: AM
authors.lastname: Kalergis
mesh_terms: D000818:Animals; D017951:Antigen Presentation / Q000235:genetics / Q000276:immunology; D001426:Bacterial Proteins / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D018988:Bacterial Translocation / Q000235:genetics / Q000276:immunology*; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D004847:Epithelial Cells / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D017353:Gene Deletion; D051379:Mice; D008822:Mice, Transgenic; D010587:Phagocytosis / Q000235:genetics / Q000276:immunology; D012486:Salmonella typhimurium / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000472:pathogenicity*; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000382:microbiology
chemical_list: D001426:Bacterial Proteins; C419942:Spi1 protein, Salmonella