Mechanisms of<i>Salmonella</i>entry into host cells

Ly, Kim; Casanova, James E.

doi:10.1111/j.1462-5822.2007.00992.x

Cited by 108 publications

(86 citation statements)

References 69 publications

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“…Salmonella can thus infect a wide range of tissues and cell types. The best-characterized Salmonella invasion process requires a type three secretion system (T3SS-1) encoded by Salmonella pathogenicity island 1 (SPI-1) (Ly & Casanova, 2007). In vivo studies with the Salmonella Dublin and Salmonella Typhimurium serovars have demonstrated that T3SS-1 is essential for intestinal colonization and is required to induce enterocolitis in bovine, rabbit and murine models (Wallis & Galyov, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…cytoplasm to manipulate the cell cytoskeleton, allowing bacterial internalization (Ly & Casanova, 2007). This entry process is referred to as the Trigger entry mechanism and has mainly been studied with epithelial cells.…”

Section: Introductionmentioning

confidence: 99%

“…The concerted activity of these bacterial effectors has been shown to promote transient actin rearrangements. For example, SopE, SopE2 and SopB act by targeting the Rho GTPase proteins Rac, Cdc42 and RhoG, whereas SipA and SipC bind to actin directly, leading to a massive actin cytoskeleton recruitment (Ly & Casanova, 2007). This actin rearrangement leads to an intense membrane ruffling which envelops the bacterium and triggers its internalization (Francis et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

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Heterogeneity of type III secretion system (T3SS)-1-independent entry mechanisms used by Salmonella Enteritidis to invade different cell types

et al. 2011

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Salmonella causes a wide range of diseases from acute gastroenteritis to systemic typhoid fever, depending on the host. To invade non-phagocytic cells, Salmonella has developed different mechanisms. The main invasion system requires a type III secretion system (T3SS) known as T3SS-1, which promotes a Trigger entry mechanism. However, other invasion factors have recently been described in Salmonella, including Rck and PagN, which were not expressed under our bacterial culture conditions. Based on these observations, we used adhesion and invasion assays to analyse the respective roles of Salmonella Enteritidis T3SS-1-dependent and -independent invasion processes at different times of infection. Diverse cell lines and cell types were tested, including endothelial, epithelial and fibroblast cells. We demonstrated that cell susceptibility to the T3SS-1-independent entry differs by a factor of nine between the most and the least permissive cell lines tested. In addition, using scanning electron and confocal microscopy, we showed that T3SS-1-independent entry into cells was characterized by a Trigger-like alteration, as for the T3SS-1-dependent entry, and also by Zipper-like cellular alteration. Our results demonstrate for what is believed to be the first time that Salmonella can induce Trigger-like entry independently of T3SS-1 and can induce Zipper-like entry independently of Rck. Overall, these data open new avenues for discovering new invasion mechanisms in Salmonella.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Heterogeneity of type III secretion system (T3SS)-1-independent entry mechanisms used by Salmonella Enteritidis to invade different cell types

et al. 2011

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“…SipC interacts with SipB to form an extracellular complex following their secretion through the SPI-1 T3SS, and they are thought to assemble into a plasma membrane-integral structure (translocon) that mediates effector delivery and facilitates effector transport (Hayward & Koronakis, 1999;Ly & Casanova, 2007;Scherer et al, 2000). In addition to its role as a component of the translocon, SipC is an actin-binding protein that nucleates actin filament formation in vitro and contributes to Salmonella-induced inflammation in vivo (Chang et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Differential expression of Salmonella type III secretion system factors InvJ, PrgJ, SipC, SipD, SopA and SopB in cultures and in mice

Gong

Bai

et al. 2010

Microbiology

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The type III secretion system (T3SS) encoded by Salmonella pathogenicity island 1 (SPI-1) is important for the invasion of epithelial cells during development of Salmonella-associated enterocolitis. It has been suggested that the level and timing of the expression of the SPI-1 T3SS proteins and effectors dictate the consequences of bacterial infection and pathogenesis. However, the expression of these proteins has not been extensively studied in vivo, especially during the later stages of salmonellosis when the infection is established. We have constructed recombinant Salmonella strains that contain a FLAG epitope inserted in-frame to genes invJ, prgJ, sipC, sipD, sopA and sopB, and investigated the expression of the tagged proteins both in vitro and in vivo during murine salmonellosis. Mice were inoculated intraperitoneally or intragastrically with the tagged Salmonella strains. At different time points post-infection, bacteria were recovered from various organs, and the expression of the tagged proteins was determined. Our results provide direct evidence that PrgJ and SipD are expressed in Salmonella colonizing the liver and ileum of infected animals at both the early and late stages of infection. Furthermore, our study has shown that the InvJ protein is expressed preferentially in Salmonella colonizing the ileum but not the liver, while SipC is expressed preferentially in Salmonella colonizing the liver but not the ileum. Thus, Salmonella appears to express different SPI-1 proteins and effectors when colonizing specific tissues. Our results suggest that differential expression of these proteins may be important for tissue-specific aspects of bacterial pathogenesis such as gastroenterititis in the ileum and systemic infection in the liver.

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“…Both of these T3SSs are required at different stages of infection. During non-phagocytic cell invasion, the SPI-1 T3SS is activated and translocates several effector proteins into host cells to induce actin polymerization and membrane ruffling (Ly & Casanova, 2007), while the SPI-2 T3SS is important for intracellular survival and replication within macrophages (Ochman & Groisman, 1996). The SPI-1-associated protein InvE is essential for bacterial internalization and controls the secretion of translocases (SipB, SipC and SipD) of the SPI-1 T3SS (Ginocchio et al, 1992;Kubori & Galán, 2002).…”

Section: Introductionmentioning

confidence: 99%

Molecular characterization of the InvE regulator in the secretion of type III secretion translocases in Salmonella enterica serovar Typhimurium

et al. 2013

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The type III secretion systems (T3SSs) are exploited by many Gram-negative pathogenic bacteria to deliver a set of effector proteins into the host cytosol during cell entry. The T3SS of Salmonella enterica serovar Typhimurium is composed of more than 20 proteins that constitute the membrane-associated base, the needle and the tip complex at the distal end of the T3SS needle. Membrane docking and piercing between the T3SS and host cells is followed by the secretion of effector proteins. Therefore, a secretion hierarchy among the substrates of the T3SS is required. The secretion of the pore-forming translocase proteins SipB, SipC and SipD is controlled by the T3SS regulator protein, InvE. During an attempt to identify the regions of InvE that are involved in T3SS regulation, it was observed that the secretion of SipB, SipC and SipD was inhibited when the C-terminal 52 amino acids were removed from InvE. In addition, InvE derivatives lacking the Nterminal 30 and 100 residues were unable to secrete translocases into the culture medium. Interestingly, in the absence of the N-terminal 180 residues of InvE, SipD is unstable, resulting in the hypersecretion of SipB. We also found that both the type III secretion signals of SipB and SptP were functionally interchangeable with the first 30 amino acids of InvE, which could allow the secretion of a reporter protein. These results indicate that InvE may have two functional domains responsible for regulating the secretion of translocases: an N-terminal secretion signal and a Cterminal regulatory domain.

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Mechanisms ofSalmonellaentry into host cells

Cited by 108 publications

References 69 publications

Heterogeneity of type III secretion system (T3SS)-1-independent entry mechanisms used by Salmonella Enteritidis to invade different cell types

Heterogeneity of type III secretion system (T3SS)-1-independent entry mechanisms used by Salmonella Enteritidis to invade different cell types

Differential expression of Salmonella type III secretion system factors InvJ, PrgJ, SipC, SipD, SopA and SopB in cultures and in mice

Molecular characterization of the InvE regulator in the secretion of type III secretion translocases in Salmonella enterica serovar Typhimurium

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