Caspase‐3‐dependent phagocyte death during systemic <i>Salmonella enterica</i> serovar <i>Typhimurium</i> infection of mice

Grant, A.; Sheppard, Mark; Deardon, Rob; Brown, Sam P.; Foster, Gemma; Bryant, Clare E.; Maskell, Duncan J.; Mastroeni, Pietro

doi:10.1111/j.1365-2567.2008.02814.x

Cited by 31 publications

(36 citation statements)

References 32 publications

(56 reference statements)

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“…Caspase-3-dependent phagocyte apoptosis during systemic S. typhimurium infection of mice has been reported. 9 Mitochondria are an important regulator of apoptosis and undergo major changes during apoptotic cell death that is induced by apoptotic stimuli. Early in the induction of apoptosis, a loss of mitochondrial Dy m can be detected.…”

Section: S Typhi Plasmid Induces Macrophage Apoptosismentioning

confidence: 99%

“…Some studies have shown that S. typhi and Salmonella enterica serovar Typhimurium (S. typhimurium) can mediate macrophage apoptosis. [6][7][8][9][10] The virulence of Salmonella strains in humans and other animals is frequently serovar specific. S. typhi causes typhoid fever only in humans, but no disease is associated with experimental infections in mice.…”

Section: Introductionmentioning

confidence: 99%

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A Salmonella enterica serovar Typhi plasmid induces rapid and massive apoptosis in infected macrophages

et al. 2010

Cell Mol Immunol

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pR ST98 is a chimeric plasmid isolated from Salmonella enterica serovar Typhi (S. typhi) that mediates the functions of drug resistance and virulence. Previously, we reported that Salmonella plasmid virulence (spv) genes were present in S. typhi. In our current study, we investigated whether plasmid pR ST98 exhibits significant cytotoxicity in macrophages. pR ST98 was transferred into the avirulent Salmonella enterica serovar Typhimurium (S. typhimurium) strain RIA to create the transconjugant pR ST98 /RIA. The standard S. typhimurium virulent strain SR-11, which carries a 100-kb virulence plasmid, was used as a positive control. The bacterial strains were incubated with a murine macrophage-like cell line (J774A.1) in vitro. Apoptosis of J774A.1 cells was examined by electron microscopy and flow cytometry after annexin-V/propidium iodide labeling, and the survival of Salmonella strains in J774A.1 cells was determined. Results showed that macrophages infected with strain pR ST98 /RIA displayed greater levels of apoptosis than those infected with RIA and that pR ST98 may increase bacterial survival in macrophages. Further studies showed that the pR ST98 -induced death of macrophages was associated with the loss of mitochondrial membrane potential and that pR ST98 may activate caspase-9 and then caspase-3. The research data indicate that the virulence of bacteria that contain the pR ST98 plasmid is enhanced; the presence of this plasmid increases the survival of the bacterial pathogen and acts through the mitochondrial pathway to mediate macrophage apoptosis.

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Section: S Typhi Plasmid Induces Macrophage Apoptosismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A Salmonella enterica serovar Typhi plasmid induces rapid and massive apoptosis in infected macrophages

et al. 2010

Cell Mol Immunol

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“…Recently, several cases of observed phenotypic heterogeneity in bacterial populations have been suggested to be 'bet hedging' [3,[6][7][8][9][10][11][12][13][14][15][16][17][18][19]. Apparently, bet hedging is used by molecular and cell biologists to describe the observation that microorganisms potentially increase the continuity of their DNA by displaying different phenotypes within one population.…”

Section: Introductionmentioning

confidence: 99%

Bet hedging or not? A guide to proper classification of microbial survival strategies

2011

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Bacteria have developed an impressive ability to survive and propagate in highly diverse and changing environments by evolving phenotypic heterogeneity. Phenotypic heterogeneity ensures that a subpopulation is well prepared for environmental changes. The expression bet hedging is commonly (but often incorrectly) used by molecular biologists to describe any observed phenotypic heterogeneity. In evolutionary biology, however, bet hedging denotes a risk‐spreading strategy displayed by isogenic populations that evolved in unpredictably changing environments. Opposed to other survival strategies, bet hedging evolves because the selection environment changes and favours different phenotypes at different times. Consequently, in bet hedging populations all phenotypes perform differently well at any time, depending on the selection pressures present. Moreover, bet hedging is the only strategy in which temporal variance of offspring numbers per individual is minimized. Our paper aims to provide a guide for the correct use of the term bet hedging in molecular biology.

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“…Apoptosis of macrophages in the liver is observed during systemic Salmonella infection (65)(66)(67). This observation raises a hypothesis that apoptotic host cell death might constitute a mechanism allowing bacterial spread to new cells that occurs in the context of a far more active necrotic cell death process, ensuring an ongoing protective intracellular environment in which a subset of bacteria can avoid detection and targeting by the humoral branch of the immune system (68)(69)(70).…”

Section: Discussionmentioning

confidence: 99%

“…This observation raises a hypothesis that apoptotic host cell death might constitute a mechanism allowing bacterial spread to new cells that occurs in the context of a far more active necrotic cell death process, ensuring an ongoing protective intracellular environment in which a subset of bacteria can avoid detection and targeting by the humoral branch of the immune system (68)(69)(70). In cell culture, Salmonella-induced apoptosis requires the activation of TLR4 by bacterial LPS (65,71). Previous reports demonstrated that phosphorylated activated IRAK-1 also promotes downstream apoptosis (12,13,68).…”

Section: Discussionmentioning

confidence: 99%

Salmonella Virulence Factor SsrAB Regulated Factor Modulates Inflammatory Responses by Enhancing the Activation of NF-κB Signaling Pathway

Lei

Wang

Xia

et al. 2016

The Journal of Immunology

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Effector proteins encoded by Salmonella pathogenicity islands play a key role in promoting bacterial intracellular survival, colonization, and pathogenesis. In this study, we investigated the function of the virulence-associated effector SrfA (SsrAB regulated factor) both in macrophages in vitro and in infected mice in vivo. SrfA was secreted into the cytoplasm during S. Typhimurium infection and disassociated IL-1R–associated kinase-1 (IRAK-1) from the IRAK-1–Toll interacting protein (Tollip) complex by interacting with Tollip. The released IRAK-1 was phosphorylated and subsequently activated the NF-κB signaling pathway, which enhanced the LPS-induced expression of inflammatory cytokines, such as IL-8, IL-1β, and TNF-α. The coupling of ubiquitin to endoplasmic reticulum degradation aa 183–219 domain of Tollip is the binding region for SrfA, and both the MDaa207–226 and CTaa357–377 regions of SrfA mediate binding to Tollip and NF-κB signaling activation. Deletion of SrfA in S. Typhimurium had no notable effects on its replication but impaired the induction of NF-κB activation in infected macrophages. The mice infected with srfA-deficient bacteria exhibited a decreased inflammatory response and an increased survival rate compared with those infected with wild-type S. Typhimurium. We conclude that SrfA is a novel Salmonella virulence effector that helps modulate host inflammatory responses by promoting NF-κB signaling activation.

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Caspase‐3‐dependent phagocyte death during systemic Salmonella enterica serovar Typhimurium infection of mice

Cited by 31 publications

References 32 publications

A Salmonella enterica serovar Typhi plasmid induces rapid and massive apoptosis in infected macrophages

A Salmonella enterica serovar Typhi plasmid induces rapid and massive apoptosis in infected macrophages

Bet hedging or not? A guide to proper classification of microbial survival strategies

Salmonella Virulence Factor SsrAB Regulated Factor Modulates Inflammatory Responses by Enhancing the Activation of NF-κB Signaling Pathway

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