Article

Expression of δ-toxin by Staphylococcus aureus mediates escape from phago-endosomes of human epithelial and endothelial cells in the presence of β-toxin.

FunGene-Competence Center for Functional Genomics, Ernst-Moritz-Arndt University, F.-L.-Jahnstrasse 15, Greifswald, Germany.
Cellular Microbiology (impact factor: 5.46). 10/2010; 13(2):316-29. DOI:10.1111/j.1462-5822.2010.01538.x pp.316-29
Source: PubMed

ABSTRACT Staphylococcus aureus is able to invade non-professional phagocytes by interaction of staphylococcal adhesins with extracellular proteins of mammalian cells and eventually resides in acidified phago-endosomes. Some staphylococcal strains have been shown to subsequently escape from this compartment. A functional agr quorum-sensing system is needed for phagosomal escape. However, the nature of this agr dependency as well as the toxins involved in disruption of the phagosomal membrane are unknown. Using a novel technique to detect vesicular escape of S. aureus, we identified staphylococcal virulence factors involved in phagosomal escape. Here we show that a synergistic activity of the cytolytic peptide, staphylococcal δ-toxin and the sphingomyelinase β-toxin enable the phagosomal escape of staphylococci in human epithelial as well as in endothelial cells. The agr dependency of this process can be directly explained by the location of the structural gene for δ-toxin within the agr effector RNAIII.

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Keywords

agr dependency
 
agr effector RNAIII
 
compartment
 
disruption
 
endothelial cells
 
functional agr quorum-sensing system
 
human epithelial
 
mammalian cells
 
novel technique
 
staphylococcal adhesins
 
staphylococcal strains
 
staphylococcal virulence factors
 
staphylococcal δ-toxin
 
Staphylococcus aureus
 
structural gene
 
vesicular
 
δ-toxin