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

Susan M. Bueno, Aniela Wozniak, Eduardo D. Leiva, Sebastián A. Riquelme, Leandro J. Carreño, Wolf Dietrich Hardt, Claudia A. Riedel, Alexis M. Kalergis

Resultado de la investigación: Article

28 Citas (Scopus)

Resumen

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 (ΔInvC) 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 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.

Idioma originalEnglish
Páginas (desde-hasta)273-287
Número de páginas15
PublicaciónImmunology
Volumen130
N.º2
DOI
EstadoPublished - jun 2010

Huella dactilar

Genomic Islands
Salmonella
Dendritic Cells
Epithelial Cells
Salmonella enterica
Antigen Presentation
Phagocytes
Helper-Inducer T-Lymphocytes
Phagocytosis
Bacteria
T-Lymphocytes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Citar esto

Bueno, S. M., Wozniak, A., Leiva, E. D., Riquelme, S. A., Carreño, L. J., Hardt, W. D., ... Kalergis, A. M. (2010). Salmonella pathogenicity island 1 differentially modulates bacterial entry to dendritic and non-phagocytic cells. Immunology, 130(2), 273-287. https://doi.org/10.1111/j.1365-2567.2009.03233.x
Bueno, Susan M. ; Wozniak, Aniela ; Leiva, Eduardo D. ; Riquelme, Sebastián A. ; Carreño, Leandro J. ; Hardt, Wolf Dietrich ; Riedel, Claudia A. ; Kalergis, Alexis M. / Salmonella pathogenicity island 1 differentially modulates bacterial entry to dendritic and non-phagocytic cells. En: Immunology. 2010 ; Vol. 130, N.º 2. pp. 273-287.
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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 (ΔInvC) 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 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.",
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Bueno, SM, Wozniak, A, Leiva, ED, Riquelme, SA, Carreño, LJ, Hardt, WD, Riedel, CA & Kalergis, AM 2010, 'Salmonella pathogenicity island 1 differentially modulates bacterial entry to dendritic and non-phagocytic cells', Immunology, vol. 130, n.º 2, pp. 273-287. https://doi.org/10.1111/j.1365-2567.2009.03233.x

Salmonella pathogenicity island 1 differentially modulates bacterial entry to dendritic and non-phagocytic cells. / Bueno, Susan M.; Wozniak, Aniela; Leiva, Eduardo D.; Riquelme, Sebastián A.; Carreño, Leandro J.; Hardt, Wolf Dietrich; Riedel, Claudia A.; Kalergis, Alexis M.

En: Immunology, Vol. 130, N.º 2, 06.2010, p. 273-287.

Resultado de la investigación: Article

TY - JOUR

T1 - Salmonella pathogenicity island 1 differentially modulates bacterial entry to dendritic and non-phagocytic cells

AU - Bueno, Susan M.

AU - Wozniak, Aniela

AU - Leiva, Eduardo D.

AU - Riquelme, Sebastián A.

AU - Carreño, Leandro J.

AU - Hardt, Wolf Dietrich

AU - Riedel, Claudia A.

AU - Kalergis, Alexis M.

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N2 - 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 (ΔInvC) 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 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.

AB - 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 (ΔInvC) 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 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.

KW - Bacteria/bacterial immunity

KW - Dendritic cells

KW - Phagocytosis

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