scholarly journals Identification of a Peptide-Pheromone that Enhances Listeria monocytogenes Escape from Host Cell Vacuoles

2015 ◽  
Vol 11 (3) ◽  
pp. e1004707 ◽  
Author(s):  
Bobbi Xayarath ◽  
Francis Alonzo ◽  
Nancy E. Freitag
Keyword(s):  
Listeria Monocytogenes ◽  
Host Cell ◽  
Peptide Pheromone

scholarly journals Infection with Listeria monocytogenes impairs sialic acid addition to host cell glycoproteins.

1994 ◽  
Vol 180 (6) ◽  
pp. 2137-2145 ◽  
Author(s):  
M S Villanueva ◽  
C J Beckers ◽  
E G Pamer
Keyword(s):  
Listeria Monocytogenes ◽  
Sialic Acid ◽  
Host Cell ◽  
Mhc Class I ◽  
Acid Content ◽  
Class I ◽  
Sialic Acid Content ◽  
Infected Cells ◽  
The Impact ◽  
Glycosylation Defect

Listeria monocytogenes is a facultative intracellular bacterium that causes severe disease in neonates and immunocompromised adults. Although entry, multiplication, and locomotion of Listeria in the cytosol of infected cells are well described, the impact of such infection on the host cell is unknown. In this report, we investigate the effect of L. monocytogenes infection on MHC class I synthesis, processing, and intracellular trafficking. We show that L. monocytogenes infection interferes with normal processing of N-linked oligosaccharides on the major histocompatibility complex (MHC) class I heavy chain molecule, H-2Kd, resulting in a reduced sialic acid content. The glycosylation defect is more pronounced as the infection progresses and results from interference with the addition of sialic acid rather than its removal by a neuraminidase. The effect is found in two different cell lines and is not limited to MHC class I molecules since CD45, a surface glycoprotein, and LGP120, a lysosomal glycoprotein, are similarly affected by L. monocytogenes infection. The glycosylation defect is specific for infection by L. monocytogenes since neither Trypanosoma cruzi nor Yersinia enterocolitica, two other intracellular pathogens, reproduces the effect. The resultant hyposialylation of H-2Kd does not impair its surface expression in infected cells. Diminished sialic acid content of surface glycoproteins may enhance host-defense by increasing susceptibility to lysis and promoting clearance of Listeria-infected cells.

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

mBio ◽  
2018 ◽  
Vol 9 (1) ◽  
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.

scholarly journals Intracellular Gene Expression Profile of Listeria monocytogenes

2006 ◽  
Vol 74 (2) ◽  
pp. 1323-1338 ◽  
Author(s):  
Som Subhra Chatterjee ◽  
Hamid Hossain ◽  
Sonja Otten ◽  
Carsten Kuenne ◽  
Katja Kuchmina ◽  
...  
Keyword(s):  
Gene Expression ◽  
Listeria Monocytogenes ◽  
Host Cell ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Intracellular Survival ◽  
Host Cells ◽  
Wall Structure ◽  
Glucose Limitation ◽  
Serotype 4B

ABSTRACT Listeria monocytogenes is a gram-positive, food-borne microorganism responsible for invasive infections with a high overall mortality. L. monocytogenes is among the very few microorganisms that can induce uptake into the host cell and subsequently enter the host cell cytosol by breaching the vacuolar membrane. We infected the murine macrophage cell line P388D1 with L. monocytogenes strain EGD-e and examined the gene expression profile of L. monocytogenes inside the vacuolar and cytosolic environments of the host cell by using whole-genome microarray and mutant analyses. We found that ∼17% of the total genome was mobilized to enable adaptation for intracellular growth. Intracellularly expressed genes showed responses typical of glucose limitation within bacteria, with a decrease in the amount of mRNA encoding enzymes in the central metabolism and a temporal induction of genes involved in alternative-carbon-source utilization pathways and their regulation. Adaptive intracellular gene expression involved genes that are associated with virulence, the general stress response, cell division, and changes in cell wall structure and included many genes with unknown functions. A total of 41 genes were species specific, being absent from the genome of the nonpathogenic Listeria innocua CLIP 11262 strain. We also detected 25 genes that were strain specific, i.e., absent from the genome of the previously sequenced L. monocytogenes F2365 serotype 4b strain, suggesting heterogeneity in the gene pool required for intracellular survival of L. monocytogenes in host cells. Overall, our study provides crucial insights into the strategy of intracellular survival and measures taken by L. monocytogenes to escape the host cell responses.

scholarly journals Listeria monocytogenes: The Impact of Cell Death on Infection and Immunity

Pathogens ◽  
2018 ◽  
Vol 7 (1) ◽  
pp. 8 ◽  
Author(s):  
Courtney McDougal ◽  
John-Demian Sauer
Keyword(s):  
Cell Death ◽  
Listeria Monocytogenes ◽  
Host Cell ◽  
Acute Infection ◽  
Host Cells ◽  
Cell Mediated Immunity ◽  
Cell Death Pathways ◽  
Host Cell Death ◽  
The Impact

Listeria monocytogenes has evolved exquisite mechanisms for invading host cells and spreading from cell-to-cell to ensure maintenance of its intracellular lifecycle. As such, it is not surprising that loss of the intracellular replication niche through induction of host cell death has significant implications on the development of disease and the subsequent immune response. Although L. monocytogenes can activate multiple pathways of host cell death, including necrosis, apoptosis, and pyroptosis, like most intracellular pathogens L. monocytogenes has evolved a series of adaptations that minimize host cell death to promote its virulence. Understanding how L. monocytogenes modulates cell death during infection could lead to novel therapeutic approaches. In addition, as L. monocytogenes is currently being developed as a tumor immunotherapy platform, understanding how cell death pathways influence the priming and quality of cell-mediated immunity is critical. This review will focus on the mechanisms by which L. monocytogenes modulates cell death, as well as the implications of cell death on acute infection and the generation of adaptive immunity.

scholarly journals Time-Resolved Proteome Analysis of Listeria monocytogenes during Infection Reveals the Role of the AAA+ Chaperone ClpC for Host Cell Adaptation

mSystems ◽  
2021 ◽  
Author(s):  
Marlène S. Birk ◽  
Rina Ahmed-Begrich ◽  
Stefan Tran ◽  
Alexander K. W. Elsholz ◽  
Christian K. Frese ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Host Cell ◽  
Pathogenic Bacteria ◽  
Proteome Analysis ◽  
Infection Process ◽  
Time Resolved ◽  
Cell Adaptation ◽  
Proteome Level ◽  
Adaptation Processes

Survival and proliferation of pathogenic bacteria inside the host depend on their ability to adapt to the changing environment. Profiling the underlying changes on the bacterial proteome level during the infection process is important to gain a better understanding of the pathogenesis and the host-dependent adaptation processes.

scholarly journals Histone H3 deacetylation promotes host cell viability for efficient infection by Listeria monocytogenes

2021 ◽  
Vol 17 (12) ◽  
pp. e1010173
Author(s):  
Matthew J. G. Eldridge ◽  
Mélanie A. Hamon
Keyword(s):  
Dna Damage ◽  
Listeria Monocytogenes ◽  
Cell Viability ◽  
Host Cell ◽  
Histone H3 ◽  
Bacterial Pathogen ◽  
Genome Integrity ◽  
Nucleic Acid Binding ◽  
Acid Binding Protein ◽  
Common Strategy

For many intracellular bacterial pathogens manipulating host cell survival is essential for maintaining their replicative niche, and is a common strategy used to promote infection. The bacterial pathogen Listeria monocytogenes is well known to hijack host machinery for its own benefit, such as targeting the host histone H3 for modification by SIRT2. However, by what means this modification benefits infection, as well as the molecular players involved, were unknown. Here we show that SIRT2 activity supports Listeria intracellular survival by maintaining genome integrity and host cell viability. This protective effect is dependent on H3K18 deacetylation, which safeguards the host genome by counteracting infection-induced DNA damage. Mechanistically, infection causes SIRT2 to interact with the nucleic acid binding protein TDP-43 and localise to genomic R-loops, where H3K18 deacetylation occurs. This work highlights novel functions of TDP-43 and R-loops during bacterial infection and identifies the mechanism through which L. monocytogenes co-opts SIRT2 to allow efficient infection.

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