Salmonella pathogenicity island 1 differentially modulates bacterial entry to dendritic and non‐phagocytic cells

Abstract

SummarySalmonella 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 (DInvC) 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 DInvC mutant strain retained the capacity to avoid antigen presentation to T cells. However, mice infected with the DInvC 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.

Proteomic analysis of porcine mesenteric lymph-nodes after Salmonella typhimurium infection

“…Distinct to mice, S. typhimurium generally causes little or no systemic involvement in pigs [17]. Nevertheless, in our in vivo model we observed in MLN the presence of the pathogen associated to the cytoplasm of infiltrated phagocytes, in concordance with previously reported evidences that, in mice, S. typhimurium is shuttled to MLN by infected phagocytes [18,19]. Since major protein changes were detected at 2 dpi, coinciding with a higher presence of S. typhimurium in infiltrated phagocytes, it could be inferred that proteome response of porcine MLN to the infection is strongly related to changes in tissue cellularity and pathogen burden.…”

Impact ofSalmonella entericaType III Secretion System Effectors on the Eukaryotic Host Cell

“…Central to the pathogenesis of Salmonella is its ability to invade intestinal cells: M-cells, epithelial cells, and dendritic cells [9][10][11]. The best-characterized Salmonella invasion mechanism requires T3SS1 that initiates a process known as the "trigger" mechanism.…”

Cytosporone B, an Inhibitor of the Type III Secretion System of Salmonella enterica Serovar Typhimurium

“…The compounds with strong inhibitory effects on the secretion of SPI-1 effectors were further evaluated in terms of their effects on SPI-1-mediated invasion, as the invasion of Salmonella into host cells was predominately related to SPI-1 (55,56). Because the invasion assay was cell based, we first determined the cytotoxicity of the compounds secocurvularin, C5, and Csn-B on HeLa cells by MTT assay (see Fig.…”