Reduced adherence and host cell invasion by methicillin-resistant Staphylococcus aureus expressing the surface protein Pls.

@article{Juuti2004ReducedAA,
  title={Reduced adherence and host cell invasion by methicillin-resistant Staphylococcus aureus expressing the surface protein Pls.},
  author={Katri M Juuti and Bhanu Sinha and Cornelia Werbick and Georg Peters and Pentti I Kuusela},
  journal={The Journal of infectious diseases},
  year={2004},
  volume={189 9},
  pages={
          1574-84
        }
}
Pls, the surface protein of methicillin-resistant Staphylococcus aureus (MRSA), prevents adhesion of clinical strain 1061 to immobilized fibronectin (Fn) and immunoglobulin G (IgG). Invasion of mammalian cells by S. aureus depends on Fn-mediated binding of staphylococcal Fn-binding proteins to host cell beta (1)-integrins. In the present study, we show that, for 10 clinical Pls-positive (Pls(+)) MRSA strains, adhesion to immobilized Fn, fibrinogen (Fg), IgG, and laminin, as well as binding to… 
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Expression of Pls (plasmin sensitive) in Staphylococcus aureus negative for pls reduces adherence and cellular invasion and acts by steric hindrance.
BACKGROUND The methicillin-resistant Staphylococcus aureus (MRSA) surface protein Pls (plasmin sensitive) reduces adhesion to host proteins and cellular invasiveness by an unknown mechanism that…
Staphylococcal chromosomal cassette mec type I, spa type, and expression of Pls are determinants of reduced cellular invasiveness of methicillin-resistant Staphylococcus aureus isolates.
TLDR
3 properties--pls/Pls, SCCmec type, and spa type--strongly predicted the cellular invasiveness of MRSA strains, as indicated by good clustering.
The Surface Protein Pls of Methicillin-Resistant Staphylococcus aureus Is a Virulence Factor in Septic Arthritis
TLDR
Results show that Pls is a virulence factor for septic arthritis and sepsis, and inoculated with a pls knockout mutant developed a much milder arthritis and showed less grave weight reduction than mice infected with the wild-type Pls+ clinical isolate.
The Plasmin-Sensitive Protein Pls in Methicillin-Resistant Staphylococcus aureus (MRSA) Is a Glycoprotein
TLDR
Functional characterization revealed that Pls can confer increased biofilm formation, which seems to involve two distinct mechanisms, and sugar modifications may represent promising new targets for novel therapeutic or prophylactic measures against life-threatening S. aureus infections.
Truncation of Fibronectin-Binding Proteins in Staphylococcus aureus Strain Newman Leads to Deficient Adherence and Host Cell Invasion Due to Loss of the Cell Wall Anchor Function
TLDR
It is shown that both fnbANewman and fnbBNewman contain a centrally located point mutation resulting in a stop codon that leads to a truncation of both FnBPs at the end of the C domain at identical positions, which led to a loss of FnBP-dependent functions.
Role of SrtA in Pathogenicity of Staphylococcus lugdunensis
TLDR
The functionality of S. lugdunensis SrtA in anchoring LPXTG substrates to the cell wall let us define it as the pathogen’s housekeeping sortase.
Staphylococcus aureus—Eukaryotic Cell Interactions
TLDR
It was demonstrated that staphylococci adhere to endovascular tissue and endothelial cells grown in tissue culture more avidly than do other bacterial species, and the bacterial species most commonly associated with acute bacterial endocarditis were also the most adherent.
Surface Proteins of Staphylococcus aureus.
TLDR
The surface of Staphylococcus aureus is decorated with over 20 proteins that are covalently anchored to peptidoglycan by the action of sortase A, and the study of genetically manipulated strains using animal infection models has shown that many CWA proteins contribute to pathogenesis.
Staphylococcus aureus surface proteins involved in adaptation to oxacillin identified using a novel cell shaving approach.
TLDR
Results show that S. aureus modifies surface architecture in response to antibiotic adaptation, and increased resistance to β-lactam antibiotics was observed, but adaptation to oxacillin did not confer multidrug resistance.
Mechanism and consequences of invasion of endothelial cells by Staphylococcus aureus.
TLDR
Surprisingly, induction of apoptosis in human endothelial cells is more complex than previously thought, since it appears to involve multiple virulence factors.
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References

SHOWING 1-10 OF 61 REFERENCES
Heterologously Expressed Staphylococcus aureusFibronectin-Binding Proteins Are Sufficient for Invasion of Host Cells
TLDR
FnBP-coated polystyrene beads were internalized by 293 cells, demonstrating that FnBPs are sufficient for invasion of host cells without the need for (S. aureus-specific) coreceptors, and confer invasiveness to noninvasive, apathogenic gram-positive cocci.
Clinical isolates of Staphylococcus aureus exhibit diversity in fnb genes and adhesion to human fibronectin.
TLDR
The findings suggest that the interplay between pathogenesis and a single virulence determinant is unlikely to be a uniform process across a spectrum of infections, and confirms the need to extend the study of staphylococcal pathogenesis from the laboratory to non-uniform populations of clinically relevant isolates.
Increased Virulence of a Fibronectin-Binding Protein Mutant of Staphylococcus aureus in a Rat Model of Pneumonia
TLDR
Fibronectin-binding protein-mediated internalization into alveolar epithelial cells is not a virulence mechanism in a rat model of pneumonia, and the data suggest that fibronectIn-binding proteins decrease the virulence of S. aureus in pneumonia.
Fibronectin Binding Protein and Host Cell Tyrosine Kinase Are Required for Internalization of Staphylococcus aureus by Epithelial Cells
TLDR
Results indicate that S. aureus invades nonprofessional phagocytes by a mechanism requiring interaction between FnBP and the host cell, leading to signal transduction and subsequent rearrangement of the host Cell cytoskeleton.
Cellular invasion by Staphylococcus aureus involves a fibronectin bridge between the bacterial fibronectin-binding MSCRAMMs and host cell beta1 integrins.
TLDR
A model of S. aureus invasion is put forward in which host FN forms a bridge between the bacterial Fnbps and host cell beta1 integrins, leading to bacterial uptake.
Fibronectin‐binding protein acts as Staphylococcus aureus invasin via fibronectin bridging to integrin α5β1
TLDR
FnBPs acted as S. aureus invasins and host cell integrin α5β1 served as host cell receptor, which interacted with staphylococcal FnBPs through cellular or soluble fibronectin, which lost invasiveness for epithelial cells, endothelial cells and fibroblasts.
Introduction of the mec Element (Methicillin Resistance) into Staphylococcus aureus Alters In Vitro Functional Activities of Fibrinogen and Fibronectin Adhesins
TLDR
The chromosomal insertion of themec element into genetically defined strains of S. aureus impairs the in vitro functional activities of fibrinogen or fibronectin adhesins without altering their production.
Extracellular Adherence Protein from Staphylococcus aureus Enhances Internalization into Eukaryotic Cells
TLDR
It is shown that Eap (extracellular adherence protein) plays a role in the internalization process of Staphylococcus aureus into eukaryotic cells, and a novel internalization pathway for S. a Aureus is proposed in which Eap plays an enhancing role.
Adherence of Staphylococcus aureus is enhanced by an endogenous secreted protein with broad binding activity.
TLDR
Binding of S. aureus to fibroblasts and epithelial cells was significantly enhanced by addition of Eap, presumably due to its affinity both for plasma proteins on the cells and for the bacteria.
The Staphylococcus aureus surface protein SasG and its homologues promote bacterial adherence to human desquamated nasal epithelial cells.
TLDR
It is shown that the S. aureus surface protein SasG, identified previously by in silico analysis of genome sequences, and two homologous proteins, Pls of S.aureus and AAP of Staphylococcus epidermidis, also promote bacterial adherence to nasal epithelial cells.
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