Faculty Opinions recommendation of Strain-Specific Interactions of Listeria monocytogenes with the Autophagy System in Host Cells.

Listeria monocytogenes is a facultative intracellular bacterial pathogen that escapes from a phagosome and grows in the host cell cytosol. The pore-forming cholesterol-dependent cytolysin, listeriolysin O (LLO), mediates bacterial escape from vesicles and is ∼10-fold more active at an acidic than neutral pH. By swapping dissimilar residues from a pH-insensitive orthologue, perfringolysin O (PFO), we identified leucine 461 as unique to pathogenic Listeria and responsible for the acidic pH optimum of LLO. Conversion of leucine 461 to the threonine present in PFO increased the hemolytic activity of LLO almost 10-fold at a neutral pH. L. monocytogenes synthesizing LLO L461T, expressed from its endogenous site on the bacterial chromosome, resulted in a 100-fold virulence defect in the mouse listeriosis model. These bacteria escaped from acidic phagosomes and initially grew normally in cells and spread cell to cell, but prematurely permeabilized the host membrane and killed the cell. These data show that the acidic pH optimum of LLO results from an adaptive mutation that acts to limit cytolytic activity to acidic vesicles and prevent damage in the host cytosol, a strategy also used by host cells to compartmentalize lysosomal hydrolases.

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Cell interactions of Listeria monocytogenes L forms and peritoneal exudative cells in rats

Canadian Journal of Microbiology ◽

10.1139/m93-154 ◽

1993 ◽

Vol 39 (11) ◽

pp. 1014-1021 ◽

Cited By ~ 5

Author(s):

L. Mihailova ◽

N. Markova ◽

T. Radoucheva ◽

D. Veljanov ◽

S. Radoevska

Keyword(s):

Listeria Monocytogenes ◽

Peritoneal Cavity ◽

Electron Microscopic Examination ◽

Lavage Fluid ◽

Host Cells ◽

Electron Microscopic ◽

Cellular Defense ◽

Scanning Electron Microscopic ◽

Scanning Electron

Listeria monocytogenes 4b and its forms without cell walls (L forms of a protoplastic type) were used to study in vivo interactions with host cells. Samples of peritoneal lavage fluid were obtained from rats intraperitoneally inoculated at intervals between 1 and 15 days after challenge, for scanning electron microscopic, bacteriological, biochemical, and cytometrical investigations. Scanning electron microscopic examination revealed continuous adhesion of L forms on the macrophage surface up to 15 days after inoculation. The persistence of the L forms within the peritoneal cavity was also shown bacteriologically at all sample times, while the parental bacterial forms were isolated from the peritoneal cavity up to 7 days after challenge. The total count of peritoneal exudative cells determined by automated flow peroxidase cytometry peaked on the 15th day in animals infected with parental forms, while in animals infected with L forms the peak was lower and the macrophage population was predominant. The glycolytic and acid phosphatase activity of peritoneal exudative cells was two times higher in rats infected with L forms as compared with rats infected with the L. monocytogenes parental forms on the 3rd day after challenge. An understanding of the nature of the interactions between L forms of L. monocytogenes and peritoneal exudative cells found in vivo could be used to establish the influence of L forms on host cellular defense mechanisms.Key words: Listeria monocytogenes, L forms, peritoneal exudative cells, electron microscopy.

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Invasion of the Brain by Listeria monocytogenes Is Mediated by InlF and Host Cell Vimentin

mBio ◽

10.1128/mbio.00160-18 ◽

2018 ◽

Vol 9 (1) ◽

Cited By ~ 27

Author(s):

Pallab Ghosh ◽

Elizabeth M. Halvorsen ◽

Dustin A. Ammendolia ◽

Nirit Mor-Vaknin ◽

Mary X. D. O’Riordan ◽

...

Keyword(s):

Listeria Monocytogenes ◽

Host Cell ◽

Bacterial Pathogen ◽

Surface Protein ◽

Host Cells ◽

Intermediate Filament Protein ◽

Life Threatening ◽

Host Cell Surface ◽

Filament Protein ◽

The Brain

ABSTRACTListeria monocytogenesis a facultative intracellular bacterial pathogen that is frequently associated with food-borne infection. Of particular concern is the ability ofL. monocytogenesto breach the blood-brain barrier, leading to life-threatening meningitis and encephalitis. The mechanisms used by bacterial pathogens to infect the brain are not fully understood. Here we show thatL. monocytogenesis able to utilize vimentin for invasion of host cells. Vimentin is a type III intermediate filament protein within the cytosol but is also expressed on the host cell surface. We found thatL. monocytogenesinteraction with surface-localized vimentin promoted bacterial uptake. Furthermore, in the absence of vimentin,L. monocytogenescolonization of the brain was severely compromised in mice. TheL. monocytogenesvirulence factor InlF was found to bind vimentin and was necessary for optimal bacterial colonization of the brain. These studies reveal a novel receptor-ligand interaction that enhances infection of the brain byL. monocytogenesand highlights the importance of surface vimentin in host-pathogen interactions.IMPORTANCEListeria monocytogenesis an intracellular bacterial pathogen that is capable of invading numerous host cells during infection.L. monocytogenescan cross the blood-brain barrier, leading to life-threatening meningitis. Here we show that anL. monocytogenessurface protein, InlF, is necessary for optimal colonization of the brain in mice. Furthermore, in the absence of vimentin, a cytosolic intermediate filament protein that is also present on the surface of brain endothelial cells, colonization of the brain was significantly impaired. We further show that InlF binds vimentin to mediate invasion of host cells. This work identifies InlF as a bacterial surface protein with specific relevance for infection of the brain and underscores the significance of host cell surface vimentin interactions in microbial pathogenesis.

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Avoidance of Autophagy Mediated by PlcA or ActA Is Required for Listeria monocytogenes Growth in Macrophages

Infection and Immunity ◽

10.1128/iai.00110-15 ◽

2015 ◽

Vol 83 (5) ◽

pp. 2175-2184 ◽

Cited By ~ 51

Author(s):

Gabriel Mitchell ◽

Liang Ge ◽

Qiongying Huang ◽

Chen Chen ◽

Sara Kianian ◽

...

Keyword(s):

Listeria Monocytogenes ◽

Wild Type Strain ◽

Fold Increase ◽

Host Cells ◽

Listeriolysin O ◽

Wild Type ◽

Conjugation System ◽

Content Type ◽

A Cell ◽

Gain Access

Listeria monocytogenesis a facultative intracellular pathogen that escapes from phagosomes and grows in the cytosol of infected host cells. Most of the determinants that govern its intracellular life cycle are controlled by the transcription factor PrfA, including the pore-forming cytolysin listeriolysin O (LLO), two phospholipases C (PlcA and PlcB), and ActA. We constructed a strain that lacked PrfA but expressed LLO from a PrfA-independent promoter, thereby allowing the bacteria to gain access to the host cytosol. This strain did not grow efficiently in wild-type macrophages but grew normally in macrophages that lacked ATG5, a component of the autophagy LC3 conjugation system. This strain colocalized more with the autophagy marker LC3 (42% ± 7%) at 2 h postinfection, which constituted a 5-fold increase over the colocalization exhibited by the wild-type strain (8% ± 6%). While mutants lacking the PrfA-dependent virulence factor PlcA, PlcB, or ActA grew normally, a double mutant lacking both PlcA and ActA failed to grow in wild-type macrophages and colocalized more with LC3 (38% ± 5%). Coexpression of LLO and PlcA in a PrfA-negative strain was sufficient to restore intracellular growth and decrease the colocalization of the bacteria with LC3. In a cell-free assay, purified PlcA protein blocked LC3 lipidation, a key step in early autophagosome biogenesis, presumably by preventing the formation of phosphatidylinositol 3-phosphate (PI3P). The results of this study showed that avoidance of autophagy byL. monocytogenesprimarily involves PlcA and ActA and that either one of these factors must be present forL. monocytogenesgrowth in macrophages.

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Life of Listeria monocytogenes in the host cells' cytosol

Microbes and Infection ◽

10.1016/j.micinf.2007.05.006 ◽

2007 ◽

Vol 9 (10) ◽

pp. 1188-1195 ◽

Cited By ~ 49

Author(s):

Biju Joseph ◽

Werner Goebel

Keyword(s):

Listeria Monocytogenes ◽

Host Cells

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Engagement of heterogeneous nuclear ribonucleoprotein M with listeriolysin O induces type I interferon expression and restricts Listeria monocytogenes growth in host cells

Immunobiology ◽

10.1016/j.imbio.2012.01.009 ◽

2012 ◽

Vol 217 (10) ◽

pp. 972-981 ◽

Cited By ~ 4

Author(s):

Zheng Luo ◽

Zhonghua Li ◽

Kun Chen ◽

Ruochen Liu ◽

Xiaoqi Li ◽

...

Keyword(s):

Listeria Monocytogenes ◽

Type I Interferon ◽

Host Cells ◽

Type I ◽

Listeriolysin O ◽

Heterogeneous Nuclear Ribonucleoprotein ◽

Nuclear Ribonucleoprotein

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Invasion of Host Cells by Listeria monocytogenes

Listeria monocytogenes: Pathogenesis and Host Response ◽

10.1007/978-0-387-49376-3_8 ◽

2007 ◽

pp. 159-176

Author(s):

Javier Pizarro-Cerdà ◽

Pascale Cossart

Keyword(s):

Listeria Monocytogenes ◽

Host Cells

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Adhesion of Campylobacter jejuni Is Increased in Association with Foodborne Bacteria

Microorganisms ◽

10.3390/microorganisms8020201 ◽

2020 ◽

Vol 8 (2) ◽

pp. 201

Author(s):

Anja Klančnik ◽

Ivana Gobin ◽

Barbara Jeršek ◽

Sonja Smole Možina ◽

Darinka Vučković ◽

...

Keyword(s):

Escherichia Coli ◽

Listeria Monocytogenes ◽

Campylobacter Jejuni ◽

Biofilm Formation ◽

Risk Evaluation ◽

Acanthamoeba Castellanii ◽

Host Cells ◽

E Coli ◽

Adverse Conditions ◽

Ultrathin Sections

The aim of this study was to evaluate Campylobacter jejuni NTCT 11168 adhesion to abiotic and biotic surfaces when grown in co-culture with Escherichia coli ATCC 11229 and/or Listeria monocytogenes 4b. Adhesion of C. jejuni to polystyrene and to Caco-2 cells and Acanthamoeba castellanii was lower for at least 3 log CFU/mL compared to E. coli and L. monocytogenes. Electron micrographs of ultrathin sections revealed interactions of C. jejuni with host cells. In co-culture with E. coli and L. monocytogenes, adhesion of C. jejuni to all tested surfaces was significantly increased for more than 1 log CFU/mL. There was 10% higher aggregation for C. jejuni than for other pathogens, and high co-aggregation of co-cultures of C. jejuni with E. coli and L. monocytogenes. These data show that C. jejuni in co-cultures with E. coli and L. monocytogenes present significantly higher risk than C. jejuni as mono-cultures, which need to be taken into account in risk evaluation. C. jejuni adhesion is a prerequisite for their colonization, biofilm formation, and further contamination of the environment. C. jejuni survival under adverse conditions as a factor in their pathogenicity and depends on their adhesion to different surfaces, not only as individual strains, but also in co-cultures with other bacteria like E. coli and L. monocytogenes.

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