<i>Salmonella</i>
            -Containing Vacuoles Display Centrifugal Movement Associated with Cell-to-Cell Transfer in Epithelial Cells

Szeto, Jason; Namolovan, Anton; Osborne, Suzanne E.; Coombes, Brian K.; Brumell, John H.

doi:10.1128/iai.01275-08

Cited by 42 publications

(63 citation statements)

References 57 publications

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“…Interestingly, replication in epithelial cells can also occur in the cytosol, and although it occurs only in less than 20% of infected cells, it accounts for the majority of the net replication [61]. In addition, in epithelial cells, a subset of SCVs is not maintained at a juxtanuclear position but moves towards the cell host periphery [62]. This centrifugal movement depends upon host microtubules and kinesin and the T3SS2 PipB2 and is associated with a decrease in the T3SS1 effectors SipA and SopB [62].…”

Section: Biogenesis Of the Salmonella-containingmentioning

confidence: 99%

“…The characteristic positioning of SCV to juxtanuclear regions suggests that the kinesininhibitory action of SifA may be dominant over the effects of PipB2 at 8 to 14 h postinfection. However, at later stages of epithelial cell infection, there is an outward displacement of a significant proportion of SCVs that is dependent upon host microtubules, kinesin and PipB2, and that is involved in cellto-cell spread of Salmonella during infection [62]. Recently, it has been shown that the level of PipB2 is similar under SPI1-and SPI2-inducing conditions and that, in addition to T3SS2, this effector can use T3SS1 to be translocated into several mammalian cell types [196].…”

Section: Pipbmentioning

confidence: 99%

“…In addition, in epithelial cells, a subset of SCVs is not maintained at a juxtanuclear position but moves towards the cell host periphery [62]. This centrifugal movement depends upon host microtubules and kinesin and the T3SS2 PipB2 and is associated with a decrease in the T3SS1 effectors SipA and SopB [62]. Both escape from the vacuole and centrifugal displacement of the SCV have been associated with the ability of Salmonella to achieve cell-to-cell transfer in order to repeat the intracellular cycle [62,63].…”

Section: Biogenesis Of the Salmonella-containingmentioning

confidence: 99%

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

Ramos‐Morales

2012

ISRN Cell Biology

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Type III secretion systems are molecular machines used by many Gram-negative bacterial pathogens to inject proteins, known as effectors, directly into eukaryotic host cells. These proteins manipulate host signal transduction pathways and cellular processes to the pathogen's advantage. Salmonella enterica possesses two virulence-related type III secretion systems that deliver more than forty effectors. This paper reviews our current knowledge about the functions, biochemical activities, host targets, and impact on host cells of these effectors. First, the concerted action of effectors at the cellular level in relevant aspects of the interaction between Salmonella and its hosts is analyzed. Then, particular issues that will drive research in the field in the near future are discussed. Finally, detailed information about each individual effector is provided.

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Section: Biogenesis Of the Salmonella-containingmentioning

confidence: 99%

Section: Pipbmentioning

confidence: 99%

Section: Biogenesis Of the Salmonella-containingmentioning

confidence: 99%

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

Ramos‐Morales

2012

ISRN Cell Biology

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“…A Salmonella sifA mutant rapidly becomes cytosolic, and its virulence is strongly attenuated in mice (19). While vacuolar lysis most probably occurs during lytic egress (see Egress Strategies Involving Lysis of the Vacuole and Host Cell), it might not be required for a mechanism of direct cell-to-cell transfer, relying on the kinesindependent repositioning of the Salmonella-containing vacuole from the juxtanuclear region to the periphery (83,141).…”

Section: Vacuole Lysis and Escape To The Cytosolmentioning

confidence: 99%

Prison Break: Pathogens' Strategies To Egress from Host Cells

Friedrich

Hagedorn

Soldati‐Favre

et al. 2012

Microbiol Mol Biol Rev

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SUMMARYA wide spectrum of pathogenic bacteria and protozoa has adapted to an intracellular life-style, which presents several advantages, including accessibility to host cell metabolites and protection from the host immune system. Intracellular pathogens have developed strategies to enter and exit their host cells while optimizing survival and replication, progression through the life cycle, and transmission. Over the last decades, research has focused primarily on entry, while the exit process has suffered from neglect. However, pathogen exit is of fundamental importance because of its intimate association with dissemination, transmission, and inflammation. Hence, to fully understand virulence mechanisms of intracellular pathogens at cellular and systemic levels, it is essential to consider exit mechanisms to be a key step in infection. Exit from the host cell was initially viewed as a passive process, driven mainly by physical stress as a consequence of the explosive replication of the pathogen. It is now recognized as a complex, strategic process termed “egress,” which is just as well orchestrated and temporally defined as entry into the host and relies on a dynamic interplay between host and pathogen factors. This review compares egress strategies of bacteria, pathogenic yeast, and kinetoplastid and apicomplexan parasites. Emphasis is given to recent advances in the biology of egress in mycobacteria and apicomplexans.

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“…Cells were also infected with WT Salmonella carrying pHG86 empty vector as a control. At selected time points post-infection, as described by Szeto et al (2009), cells were washed twice with PBS and harvested using a total of 1 ml ice-cold lysis buffer per well (1 % Triton X-100, 0.1 % SDS, 1 mM PMSF, 5 mM NaF, 5 mM NaV, 10 mg aprotinin ml 21 , 1 mg leupeptin ml 21 , 10 mg pepstatin ml 21 ). A 200 ml sample of cell lysate from each time point was used to enumerate intracellular bacteria by dilution plating.…”

mentioning

confidence: 99%

Novel role of the nitrite transporter NirC in Salmonella pathogenesis: SPI2-dependent suppression of inducible nitric oxide synthase in activated macrophages

Das

Lahiri

et al. 2009

Microbiology

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Activation of macrophages by interferon gamma (IFN-c) and the subsequent production of nitric oxide (NO) are critical for the host defence against Salmonella enterica serovar Typhimurium infection. We report here the inhibition of IFN-c-induced NO production in RAW264.7 macrophages infected with wild-type Salmonella. This phenomenon was shown to be dependent on the nirC gene, which encodes a potential nitrite transporter. We observed a higher NO output from IFN-c-treated macrophages infected with a nirC mutant of Salmonella. The nirC mutant also showed significantly decreased intracellular proliferation in a NO-dependent manner in activated RAW264.7 macrophages and in liver, spleen and secondary lymph nodes of mice, which was restored by complementing the gene in trans. Under acidified nitrite stress, a twofold more pronounced NO-mediated repression of SPI2 was observed in the nirC knockout strain compared to the wild-type. This enhanced SPI2 repression in the nirC knockout led to a higher level of STAT-1 phosphorylation and inducible nitric oxide synthase (iNOS) expression than seen with the wild-type strain. In iNOS knockout mice, the organ load of the nirC knockout strain was similar to that of the wild-type strain, indicating that the mutant is exclusively sensitive to the host nitrosative stress. Taken together, these results reveal that intracellular Salmonella evade killing in activated macrophages by downregulating IFN-c-induced NO production, and they highlight the critical role of nirC as a virulence gene.

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Salmonella -Containing Vacuoles Display Centrifugal Movement Associated with Cell-to-Cell Transfer in Epithelial Cells

Cited by 42 publications

References 57 publications

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

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

Prison Break: Pathogens' Strategies To Egress from Host Cells

Novel role of the nitrite transporter NirC in Salmonella pathogenesis: SPI2-dependent suppression of inducible nitric oxide synthase in activated macrophages

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