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Staphylococcus aureus  necrotizing pneumonia is a severe disease caused by  S. aureus  strains carrying the Panton Valentine leukocidin (PVL) genes ( luk S-PV &  luk F-PV) encoded on various bacteriophages (such as phiSLT). Clinical PVL+ strains isolated from necrotizing pneumonia display an increased attachment to matrix molecules (type I and IV collagens and laminin), a phenotype that could play a role in bacterial adhesion to damaged airway epithelium during the early stages of necrotizing pneumonia (J Infect Dis 2004; 190: 1506–15). To investigate the basis of the observed adhesion of  S. aureus  PVL+ strains, we compared the ability of PVL+ and their isogenic PVL− strains to attach to various immobilized matrix molecules. The expression of recombinant fragments of the PVL subunits and the addition of synthetic peptides indicated that the processed LukS-PV signal peptide (LukS-PV SP) was sufficient to significantly enhance the ability of  S. aureus  to attach to extracellular matrix (ECM) components. Furthermore, we showed that adhesion to ECM components was inhibited by heparin and heparan sulfates (HS) suggesting that  in vivo , HS could function as a molecular bridge between the matrix and  S. aureus  expressing the LukS-PV signal peptide. Site directed mutagenesis, biochemical and structural analyses of the LukS-PV signal peptide indicate that this peptide is present at the  S. aureus  surface, binds to HS in solid phase assay, and mediates the enhanced  S. aureus  matrix component adhesion. Our data suggests that after its cleavage by signal peptidase, the signal peptide is released from the membrane and associates to the cell wall through its unique C-terminus sequence, while its highly positively charged N-terminus is exposed on the bacterial surface, allowing its interaction with extracellular matrix-associated HS. This mechanism may provide a molecular bridge that enhances the attachment of the  S. aureus  PVL+ strains to ECM components exposed at damaged epithelial sites.

The Signal Peptide of Staphylococcus aureus Panton Valentine Leukocidin LukS Component Mediates Increased Adhesion to Heparan Sulfates