Fluxes of Ca
            <sup>2+</sup>
            and K
            <sup>+</sup>
            Are Required for the Listeriolysin O-Dependent Internalization Pathway of Listeria monocytogenes

Vadia, Stephen; Seveau, Stéphanie

doi:10.1128/iai.01067-13

Cited by 34 publications

(46 citation statements)

References 60 publications

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“…Perforation is indicated by a rapid, LLO-dependent influx of extracellular Ca 2+ upon addition of L. monocytogenes to animal cells [75]. Cell perforation can also be directly detected by measuring the entry of small cell-impermeant fluorescent dyes into host cells, as for example ethidium homodimer or propidium iodide [89, 131]. Plasma membrane perforation is a very dangerous situation for host cells, which must immediately eliminate the toxin pore in order to survive.…”

Section: Listeriolysin O Is An Extracellular Pore-forming Toxinmentioning

confidence: 99%

“…Numerous Ca 2+ -sensitive transducers are known to respond to cytosolic variations in Ca 2+ concentration; however, it is unclear how host cells sense and respond to variation in intracellular K + . Adding more complexity, the combinatorial effect of simultaneous ionic and molecular fluxes should be considered when studying how extracellular LLO controls host cell signaling [131]. …”

Section: Listeriolysin O Is An Extracellular Pore-forming Toxinmentioning

confidence: 99%

“…This study showed for the first time that a pore-forming toxin can activate bacterial internalization. This novel internalization pathway requires host cell tyrosine kinase activity, F-actin polymerization, dynamin, but is microtubule- and clathrin-independent [131]. The organization of the plasma membrane into signaling, cholesterol-rich microdomains is essential for L. monocytogenes internalization [155, 156].…”

Section: Listeriolysin O Is An Extracellular Pore-forming Toxinmentioning

confidence: 99%

“…More recent studies propose that a combination of Ca 2+ - influx and K + -efflux is required for the LLO-dependent internalization pathway. Further linking ion fluxes to bacterial internalization, cell treatment with both Ca 2+ and K + ionophores, in the absence of LLO, could induce the internalization of large cargoes such as 1 μm polystyrene beads or bacteria [131]. Thus, damaging the host cell plasma membrane emerges as an invasion strategy, shared by unrelated pathogens, that involves ion fluxes across the perforated plasma membrane.…”

Section: Listeriolysin O Is An Extracellular Pore-forming Toxinmentioning

confidence: 99%

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Multifaceted Activity of Listeriolysin O, the Cholesterol-Dependent Cytolysin of Listeria monocytogenes

Seveau

2014

MACPF/CDC Proteins - Agents of Defence, Attack and Invasion

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The cholesterol-dependent cytolysins (CDCs) are a large family of pore-forming toxins that are produced by numerous Gram-positive bacterial pathogens. These toxins are released in the extracellular environment as water-soluble monomers or dimers that bind to cholesterol-rich membranes and assemble into large pore complexes. Depending upon their concentration, the nature of the host cell and membrane (cytoplasmic or intracellular) they target, the CDCs can elicit many different cellular responses. Among the CDCs, listeriolysin O (LLO), which is a major virulence factor of the facultative intracellular pathogen Listeria monocytogenes, is involved in several stages of the intracellular lifecycle of the bacterium and displays unique characteristics. It has long been known that following L. monocytogenes internalization into host cells, LLO disrupts the internalization vacuole, enabling the bacterium to replicate into the host cell cytosol. LLO is then used by cytosolic bacteria to spread from cell to cell, avoiding bacterial exposure to the extracellular environment. Although LLO is continuously produced during the intracellular lifecycle of L. monocytogenes, several processes limit its toxicity to ensure the survival of infected cells. It was previously thought that LLO activity was limited to mediating vacuolar escape during bacterial entry and cell to cell spreading. This concept has been challenged by compelling evidence suggesting that LLO secreted by extracellular L. monocytogenes perforates the host cell plasma membrane, triggering important host cell responses. This chapter provides an overview of the well-established intracellular activity of LLO and the multiple roles attributed to LLO secreted by extracellular L. monocytogenes.

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Section: Listeriolysin O Is An Extracellular Pore-forming Toxinmentioning

confidence: 99%

Section: Listeriolysin O Is An Extracellular Pore-forming Toxinmentioning

confidence: 99%

Section: Listeriolysin O Is An Extracellular Pore-forming Toxinmentioning

confidence: 99%

Section: Listeriolysin O Is An Extracellular Pore-forming Toxinmentioning

confidence: 99%

See 2 more Smart Citations

Multifaceted Activity of Listeriolysin O, the Cholesterol-Dependent Cytolysin of Listeria monocytogenes

Seveau

2014

MACPF/CDC Proteins - Agents of Defence, Attack and Invasion

Self Cite

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“…Ca 2+ influx has been shown to promote bacterial entry, possibly through the fusion of subcortical vesicles that increase the membrane availability required for the uptake of a particle as large as a bacterium [35,36]. In addition, compartments of the endomembrane system, such as the ER, release stored Ca 2+ into the cytosol upon infection.…”

Section: Inhibition Of Lysosome Fusionmentioning

confidence: 98%

Organelle targeting during bacterial infection: insights from Listeria

Lebreton

Stavru

Cossart

2015

Trends in Cell Biology

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Listeria monocytogenes, a facultative intracellular bacterium responsible for severe foodborne infections, is now recognized as a multifaceted model in infection biology. Comprehensive studies of the molecular and cellular basis of the infection have unraveled how the bacterium crosses the intestinal and feto-placental barriers, invades several cell types in which it multiplies and moves, and spreads from cell to cell. Interestingly, although Listeria does not actively invade host cell organelles, it can interfere with their function. We discuss the effect of Listeria on the endoplasmic reticulum (ER) and the mechanisms leading to the fragmentation of the mitochondrial network and its consequences, and review the strategies used by Listeria to subvert nuclear functions, more precisely to control host gene expression at the chromatin level.

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Mechanisms protecting host cells against bacterial pore-forming toxins

Brito

Cabanes

Mesquita

et al. 2018

Cell. Mol. Life Sci.

104

129

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Pore-forming toxins (PFTs) are key virulence determinants produced and secreted by a variety of human bacterial pathogens. They disrupt the plasma membrane (PM) by generating stable protein pores, which allow uncontrolled exchanges between the extracellular and intracellular milieus, dramatically disturbing cellular homeostasis. In recent years, many advances were made regarding the characterization of conserved repair mechanisms that allow eukaryotic cells to recover from mechanical disruption of the PM membrane. However, the specificities of the cell recovery pathways that protect host cells against PFT-induced damage remain remarkably elusive. During bacterial infections, the coordinated action of such cell recovery processes defines the outcome of infected cells and is, thus, critical for our understanding of bacterial pathogenesis. Here, we review the cellular pathways reported to be involved in the response to bacterial PFTs and discuss their impact in single-cell recovery and infection.

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Fluxes of Ca ²⁺ and K ⁺ Are Required for the Listeriolysin O-Dependent Internalization Pathway of Listeria monocytogenes

Cited by 34 publications

References 60 publications

Multifaceted Activity of Listeriolysin O, the Cholesterol-Dependent Cytolysin of Listeria monocytogenes

Multifaceted Activity of Listeriolysin O, the Cholesterol-Dependent Cytolysin of Listeria monocytogenes

Organelle targeting during bacterial infection: insights from Listeria

Mechanisms protecting host cells against bacterial pore-forming toxins

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Fluxes of Ca 2+ and K + Are Required for the Listeriolysin O-Dependent Internalization Pathway of Listeria monocytogenes

Cited by 34 publications

References 60 publications

Multifaceted Activity of Listeriolysin O, the Cholesterol-Dependent Cytolysin of Listeria monocytogenes

Multifaceted Activity of Listeriolysin O, the Cholesterol-Dependent Cytolysin of Listeria monocytogenes

Organelle targeting during bacterial infection: insights from Listeria

Mechanisms protecting host cells against bacterial pore-forming toxins

Contact Info

Product

Resources

About

Fluxes of Ca ²⁺ and K ⁺ Are Required for the Listeriolysin O-Dependent Internalization Pathway of Listeria monocytogenes