The Salmonella enterica subspecies I specific centisome 7 genomic island encodes novel protein families present in bacteria living in close contact with eukaryotic cells

Folkesson, Anders; Löfdahl, Sven; Normark, Staffan

doi:10.1016/s0923-2508(02)01348-7

Cited by 104 publications

(120 citation statements)

References 23 publications

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“…While other T6SSs, such as that of P. aeruginosa and V. cholerae, have been found to have antibacterial properties, we were unable to observe this phenomenon in the S. enterica T6SS in solid LB agar-based competition assays against E. coli (data not shown) (22,33). In addition, a previous report found that deletion of the entire SCI genomic island resulted in a 50% reduction of HEp-2 epithelial cells but we were unable to observe an effect on the invasion of both HeLa and HEp-2 epithelial cells by our sciG and sciS mutants, suggesting that gut epithelial cells may not be the target of this system and that this reduction in invasion may be due to a different SCI-encoded factor (16). Interestingly, sciL in cluster 1 and rhs2 and sciX in cluster 4 were found to be upregulated in macrophages and not in HeLa epithelial cells (21).…”

Section: Figcontrasting

confidence: 51%

“…A previous report had shown that transcript levels of the icmF ortholog sciS remain low until late time points (Ͼ16 h) in macrophage infections (38). To determine whether Hcp and VrgS expression follows this pattern, we collected the contents of individual wells of infected RAW 264.7 cells at 4,8,16, and 24 h postinfection. Hcp-3 expression was evident at early time points, while VrgS, Hcp-1, and Hcp-2 expression was weak.…”

Section: Resultsmentioning

confidence: 99%

“…The ClpV ATPase is encoded by a core T6SS gene, and its abrogation results in the inability of the T6SS to assemble and secrete Hcp in V. cholerae (6). The Hcp-3 coding sequence differs significantly from those of Hcp-1 and Hcp-2, more closely resembling those of the Hcp proteins of S. bongori and Pseudomonas, and may have evolved to perform alternative functions, as is the case for the fourth S. enterica Hcp-encoding gene paralog hilE (16). Hcp-3 may therefore have an unrelated function and may be accessing the extracellular environment through an alternate secretory pathway.…”

Section: Figmentioning

confidence: 99%

“…The S. enterica subsp. enterica T6SS was first described as part of the S. enterica centisome 7 genomic island (SCI) as a contributing factor in eukaryotic pathogenesis (16). Aside from the T6SS, SCI also contains the adhesin and invasin PagN, the fimbrial gene cluster safABCD, and the transcriptional regulator sinR (15,26).…”

mentioning

confidence: 99%

“…Aside from the T6SS, SCI also contains the adhesin and invasin PagN, the fimbrial gene cluster safABCD, and the transcriptional regulator sinR (15,26). Deletion of SCI resulted in an approximately 50% reduction in internalization of HEp-2 cells that could not be complemented by PagN expression; however, complementation with safABCD or sinR was not tested (16). Disruption of SPI-6 has also been found to result in a defect in systemic dissemination in orally infected BALB/c mice (19).…”

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confidence: 99%

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Type VI Secretion System-Associated Gene Clusters Contribute to Pathogenesis of Salmonella enterica Serovar Typhimurium

2012

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ABSTRACTThe enteropathogenSalmonella entericaserovar Typhimurium employs a suite of tightly regulated virulence factors within the intracellular compartment of phagocytic host cells resulting in systemic dissemination in mice. A type VI secretion system (T6SS) withinSalmonellapathogenicity island 6 (SPI-6) has been implicated in this process; however, the regulatory inputs and the roles of noncore genes in this system are not well understood. Here we describe four clusters of noncore T6SS genes in SPI-6 based on a comparative relationship with the T6SS-3 ofBurkholderia malleiand report that the disruption of these genes results in defects in intracellular replication and systemic dissemination in mice. In addition, we show that the expression of the SPI-6-encoded Hcp and VgrG orthologs is enhanced during late stages of macrophage infection. We identify six regions that are transcriptionally active during cell infections and that have regulatory contributions from the regulators of virulence SsrB, PhoP, and SlyA. We show that levels of protein expression are very weak underin vitroconditions and that expression is not enhanced upon the deletion ofssrB,phoP,slyA,qseC,ompR, orhfq, suggesting an unknown activating factor. These data suggest that the SPI-6 T6SS has been integrated into theSalmonellaTyphimurium virulence network and customized for host-pathogen interactions through the action of noncore genes.

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Section: Figcontrasting

confidence: 51%

Section: Resultsmentioning

confidence: 99%

Section: Figmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Type VI Secretion System-Associated Gene Clusters Contribute to Pathogenesis of Salmonella enterica Serovar Typhimurium

2012

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The type VI secretion system gene cluster ofSalmonella typhimurium: Required for full virulence in mice

Liu

Guo

et al. 2012

J. Basic Microbiol.

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Type VI secretion system (T6SS) has increasingly been believed to participate in the infection process for many bacterial pathogens, but its role in the virulence of Salmonella typhimurium remains unclear. To look into this, we deleted the T6SS cluster from the genome of S. typhimurium 14028s and analyzed the phenotype of the resulting T6SS knockout mutant (T6SSKO mutant) in vitro and in vivo. We found that the T6SSKO mutant exhibited reduced capability in colonizing the spleen and liver in an in vivo colonization competition model in BALB/c mice infected by the oral route. Additionally, infection via intraperitoneal administration also showed that the T6SSKO mutant was less capable of colonizing the mouse spleen and liver than the wild-type strain. We did not detect significant differences between the T6SSKO and wild-type strains in epithelial cell invasion tests. However, in the macrophage RAW264.7 cell line, the T6SSKO mutant survived and proliferated significantly more poorly than the wild-type strain. These findings indicate that T6SS gene cluster is required for full virulence of S. typhimurium 14028s in BALB/c mice, possibly due to its roles in bacterial survival and proliferation in macrophages.

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Multiplicity of Salmonella entry mechanisms, a new paradigm for Salmonella pathogenesis

et al. 2012

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The Salmonella enterica species includes about 2600 diverse serotypes, most of which cause a wide range of food‐ and water‐borne diseases ranging from self‐limiting gastroenteritis to typhoid fever in both humans and animals. Moreover, some serotypes are restricted to a few animal species, whereas other serotypes are able to infect plants as well as cold‐ and warm‐blooded animals. An essential feature of the pathogenicity of Salmonella is its capacity to cross a number of barriers requiring invasion of a large variety of phagocytic and nonphagocytic cells. The aim of this review is to describe the different entry pathways used by Salmonella serotypes to enter different nonphagocytic cell types. Until recently, it was accepted that Salmonella invasion of eukaryotic cells required only the type III secretion system (T3SS) encoded by the Salmonella pathogenicity island‐1. However, recent evidence shows that Salmonella can cause infection in a T3SS‐1‐independent manner. Currently, two outer membrane proteins Rck and PagN have been clearly identified as Salmonella invasins. As Rck mediates a Zipper‐like entry mechanism, Salmonella is therefore the first bacterium shown to be able to induce both Zipper and Trigger mechanisms to invade host cells. In addition to these known entry pathways, recent data have shown that unknown entry routes could be used according to the serotype, the host and the cell type considered, inducing either Zipper‐like or Trigger‐like entry processes. The new paradigm presented here should change our classic view of Salmonella pathogenicity. It could also modify our understanding of the mechanisms leading to the different Salmonella‐induced diseases and to Salmonella‐host specificity.

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The Salmonella enterica subspecies I specific centisome 7 genomic island encodes novel protein families present in bacteria living in close contact with eukaryotic cells

Cited by 104 publications

References 23 publications

Type VI Secretion System-Associated Gene Clusters Contribute to Pathogenesis of Salmonella enterica Serovar Typhimurium

Type VI Secretion System-Associated Gene Clusters Contribute to Pathogenesis of Salmonella enterica Serovar Typhimurium

The type VI secretion system gene cluster ofSalmonella typhimurium: Required for full virulence in mice

Multiplicity of Salmonella entry mechanisms, a new paradigm for Salmonella pathogenesis

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