Cell Biology of the Infection by Listeria monocytogenes

Intracellular Cycle

 

 

 

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[Pizarro-Cerda-Cerda et al., Cold Spring Harbor Perspectives in Medecine 2012]

Intracellular cell cycle of L. monocytogenes. L. monocytogenes binds to epithelial host cells and promotes its own uptake in a process mediated by the two bacterial surface proteins InlA and InlB. The secreted poreforming toxin LLO (together with the bacterial phospholipases PlcA and PlcB, depending on the cell type) promotes vacuolar rupture and bacterial escape to the cytoplasm, where L. monocytogenes can replicate efficiently. Surface expression of ActA allows intracellular bacteria to polymerize host cell actin and to generate actin comet tails that propel L. monocytogenes through the cytoplasm and through membrane protrusions into neighboring cells. There, bacteria localize in a double membrane vacuole, which can be lysed by LLO, PlcA, and PlcB to start a new infection cycle.

 

 

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[Cossart, PNAS 2011]

The infection by L. monocytogenes in vitro. Schematic representation of the roles played by several virulence factors.

 

 

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[Cossart, PNAS 2011]

The infection by L. monocytogenes in vitro. The steps of the infection are schematically shown together with the bacterial factors involved and the corresponding EM images.

 

 

 

 

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[Hamon et al., Nature Reviews Microbiology 2006]

Schematic representation and electron micrographs of the Listeria monocytogenes life cycle. a) L. monocytogenes induces its entry into a non-professional phagocyte. b) Bacteria are internalized in a vacuole (also known as a phagosome). c,d) The membrane of the vacuole is disrupted by the secretion of two phospholipases, PlcA and PlcB, and the pore-forming toxin listeriolysin O. Bacteria are released into the cytoplasm, where they multiply and start to polymerize actin, as observed by the presence of the characteristic actin tails. e) Actin polymerization allows bacteria to pass into a neighbouring cell by forming protrusions in the plasma membrane. f) On entry into the neighbouring cell, bacteria are present in a double-membraned vacuole, from which they can escape to perpetuate the cycle. F-actin, filamentous actin.

 

 

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[Pizarro-Cerda-Cerda et al., The Journal of Pathology 2006]

The intracellular cycle of L. monocytogenesL. monocytogenesis able to induce its entry into target cells mainly by the activity of two invasion proteins, InlA and InlB (1). The bacteria are initially trapped within a phagocytic vacuole (2), but through the activity of the hAemolysin LLO and two other phospholipases the parasite-containing compartment is lysed. (3). Once in the cytoplasm, the freed bacteria are able to multiply and also to polymerize cellular actin  (4). L. monocytogenes moves inside the cytosol of infected cells thanks to the actin-based motility system, until it encounters the plasma membrane of the infected cell: the bacteria then push this membrane and create an invagination in the membrane of a neighbouring cell, invading it (5). The bacteria are then found in a double membrane-bound compartment (6): these membranes are lysed again due to the activity of LLO and the phospholipases (7), and L. monocytogenesis ready to start a new infection cycle.

 

 

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[Kocks et al., Cell 1992]

Thin Sections of lntracytoplasmic Wild-Type, Mutant LUTlP, and p/cB Mutant L. monocytogenes 3.5 hr Postinfection

J774 macrophages were infected for 30 min with 1.5 bacteria per cell and incubated in medium containing gentamicin.

(a) Wild-type bacterium surrounded by a dense layer of actin filaments.

(b) Wild-type bacterium associated with a long comet tail of actin.

(c and d) LUTlP mutant bacteria were not associated with microfilaments. Only some loose granular material seems to stick to the surface.

(e) LUTlP mutant bacteria multiplying freely in the cytoplasm.

(f and g) p/cB mutant bacteria associated with F-actin, similar to wild-type bacteria.

Bars represent 0.5 pm.

 

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[Tilney et al., The Journal of Cell Biology 1989]

Stages in the entry, growth, movement, and spread of Listeria from one macrophage to another. Photographs illustrating all these intermediate stages have been presented in the figures.

Updated on 13/05/2014

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