Swiss Army Pathogen: The Salmonella Entry Toolkit

Hume, Peter; Singh, Vikash; Davidson, Anthony C.; Koronakis, Vassilis

doi:10.3389/fcimb.2017.00348

Cited by 86 publications

(113 citation statements)

References 103 publications

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“…Various explanations for the caeca infection by the Δ bamB mutant strain contrary to the spleen can be put forward. First, we previously demonstrated that deletion of bamB led to a downregulation of the genes involved in the biosynthesis of the 3 T3SS of Salmonella , that is, T3SS‐1, T3SS‐2 and the flagella, which are required for systemic infection (Hume et al ., ). Bohez et al .…”

Section: Resultsmentioning

confidence: 97%

“…The frequency of spleen colonization was described for the wild type strain (C) and for the bamB mutant (D). downregulation of the genes involved in the biosynthesis of the 3 T3SS of Salmonella, that is, T3SS-1, T3SS-2 and the flagella, which are required for systemic infection (Hume et al, 2017). Bohez et al demonstrated that colonization of caeca and shedding of a ΔhilA mutant strain, which did not express the T3SS-1 related genes, was greatly decreased compared to the wild-type strain and that this strain was more or less eliminated from the chicken gut four weeks postinfection (Bohez et al, 2006).…”

Section: Systemic Infection Is Not Required For Long Term Intestinal mentioning

confidence: 99%

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Role of systemic infection, cross contaminations and super‐shedders in Salmonella carrier state in chicken

Menanteau

Kempf

Trotereau

et al. 2018

Environmental Microbiology

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Carriage of Salmonella is often associated with a high level of bacterial excretion and generally occurs after a short systemic infection. However, we do not know whether this systemic infection is required or whether the carrier-state corresponds to continuous reinfection or real persistence in caecal tissue. The use of a Salmonella Enteritidis bamB mutant demonstrated that a carrier-state could be obtained in chicken in the absence of systemic infection. The development of a new infection model in isolator showed that a marked decrease in animal reinfection and host-to-host transmission between chicks led to a heterogeneity of S. Enteritidis excretion and colonization contrary to what was observed in cages. This heterogeneity of infection was characterized by the presence of super-shedders, which constantly disseminated Salmonella to the low-shedder chicks, mainly through airborne movements of contaminated dust particles. The presence of super-shedders, in the absence of host-to-host transmission, demonstrated that constant reinfection was not required to induce a carrier-state. Finally, our results suggest that low-shedder chicks do not have a higher capability to destroy Salmonella but instead can block initial Salmonella colonization. This new paradigm opens new avenues to improve understanding of the carrier-state mechanisms and to define new strategies to control Salmonella infections.© 2018 Society for Applied Microbiology and John Wiley & Sons Ltd.

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Section: Resultsmentioning

confidence: 97%

Section: Systemic Infection Is Not Required For Long Term Intestinal mentioning

confidence: 99%

Role of systemic infection, cross contaminations and super‐shedders in Salmonella carrier state in chicken

Menanteau

Kempf

Trotereau

et al. 2018

Environmental Microbiology

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“…S . enterica deploys the Salmonella Pathogenicity Island 1‐encoded type III secretion system (SPI1‐T3SS) to invade nonphagocytic cells (Galan & Curtiss, ; reviewed in Hume, Singh, Davidson, & Koronakis, ). Within mammalian host cells, function of the Salmonella Pathogenicity Island 2‐encoded T3SS (SPI2‐T3SS) is linked to formation and maintenance of the SCV (Beuzon et al, ).…”

Section: Introductionmentioning

confidence: 99%

“…Trigger invasion mediated by STM requires the concerted action of a subset of SPI1‐T3SS effector proteins (Hume et al, ). Whereas two of the SPI1‐T3SS effectors, that is, SipA and SipC directly nucleate actin, effector proteins SopE and highly related SopE2 act as GEF for host cell Rho GTPases Rac1 and Cdc42 (Bakshi et al, ; Hardt, Chen, Schuebel, Bustelo, & Galan, ; Stender et al, ; Wood, Rosqvist, Mullan, Edwards, & Galyov, ).…”

Section: Introductionmentioning

confidence: 99%

Presence of SopE and mode of infection result in increasedSalmonella‐containing vacuole damage and cytosolic release during host cell infection bySalmonella enterica

Röder

Hensel

2020

Cellular Microbiology

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Salmonella enterica serovar Typhimurium (STM) is an invasive, facultative intracellular pathogen that has evolved sophisticated molecular mechanisms to establish an intracellular niche within a specialised vesicular compartment, the Salmonella‐containing vacuole (SCV). The loss of the SCV and release of STM into the cytosol of infected host cells was observed, and a bimodal intracellular lifestyle of STM in the SCV versus life in the cytosol is currently discussed. We set out to investigate the parameters affecting SCV integrity and cytosolic release. A fluorescent protein‐based cytosolic reporter approach was established to quantify, time‐resolved, and on a single cell level, the release of STM into the cytosol of host cells. We observed that the extent of SCV damage and cytosolic release is highly dependent on experimental conditions such as multiplicity of infection, type of host cell line, and STM strain background. Trigger invasion mediated by the Salmonella Pathogenicity Island 1‐encoded type III secretion system (SPI1‐T3SS) and its effector proteins promoted cytosolic release, whereas cytosolic bacteria were rarely observed if entry was mediated by zipper invasion. Presence of SPI1‐T3SS effector SopE was identified as major factor for damage of the SCV in the early phase after STM invasion and sopE‐expressing strains showed higher levels of cytosolic release.

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“…Through this concerted targeting of actin regulating proteins, S . Typhimurium generated membrane ruffles that eventually engulf the bacteria into newly formed host vacuoles (Galán and Zhou, ; Hume et al, ).…”

mentioning

confidence: 99%

Calponins Are Recruited to Actin‐Rich Structures Generated by Pathogenic Escherichia coli, Listeria, and Salmonella

Chua

Walker

Jin

et al. 2018

The Anatomical Record

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The ingestion of enteropathogenic Escherichia coli (EPEC), Listeria monocytogenes, or Salmonella enterica serovar Typhimurium leads to their colonization of the intestinal lumen, which ultimately causes an array of ailments ranging from diarrhea to bacteremia. Once in the intestines, these microbes generate various actin‐rich structures to attach, invade, or move within the host intestinal epithelial cells. Although an assortment of actin‐associated proteins has been identified to varying degrees at these structures, the localization of many actin stabilizing proteins have yet to be analyzed. Here, we examined the recruitment of the actin‐associated proteins, calponin 1 and 2 at EPEC pedestals, L. monocytogenes actin clouds, comet tails and listeriopods, and S. Typhimurium membrane ruffles. In other systems, calponins are known to bind to and stabilize actin filaments. In EPEC pedestals, calponin 1 was recruited uniformly throughout the structures while calponin 2 was enriched at the apical tip. During L. monocytogenes infections, calponin 1 was found through all the actin‐rich structures generated by the bacteria, while calponin 2 was only present within actin‐rich structures formed by L. monocytogenes near the host cell membrane. Finally, both calponins were found within S. Typhimurium‐generated membrane ruffles. Taken together, we have shown that although calponin 1 is recruited to actin‐rich structures formed by the three bacteria, calponin 2 is specifically recruited to only membrane‐bound actin‐rich structures formed by the bacteria. Thus, our findings suggest that calponin 2 is a novel marker for membrane‐bound actin structures formed by pathogenic bacteria. Anat Rec, 301:2103–2111, 2018. © 2018 Wiley Periodicals, Inc.

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Swiss Army Pathogen: The Salmonella Entry Toolkit

Cited by 86 publications

References 103 publications

Role of systemic infection, cross contaminations and super‐shedders in Salmonella carrier state in chicken

Role of systemic infection, cross contaminations and super‐shedders in Salmonella carrier state in chicken

Presence of SopE and mode of infection result in increasedSalmonella‐containing vacuole damage and cytosolic release during host cell infection bySalmonella enterica

Calponins Are Recruited to Actin‐Rich Structures Generated by Pathogenic Escherichia coli, Listeria, and Salmonella

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