Quantification of staphylococcal-collagen binding interactions in whole blood by use of a confocal microscopy shear-adhesion assay.

In bloodborne staphylococcal infections, bacteria and platelets often combine, forming thrombi on the subendothelium, where collagen is exposed. In this process, the collagen serves as a potential binding surface for Staphylococcus aureus. However, the extent and importance of S.

Fluid shear contributions to bacteria cell detachment initiated by a monoclonal antibody.

Receptor-mediated adhesion of bacteria to biological surfaces is a significant step leading to infection. Due to an increase in bacterial antibiotic resistance, novel methods to block and disrupt these specific interactions have gained considerable interest as possible therapeutic strategies. Recently, several monoclonal antibodies specific for the Staphylococcus aureus collagen receptor demonstrated specialized ability to displace attached cells from collagen in static assays.

Quantifying the temporal expression of the Staphylococcus aureus collagen adhesin.

The initial event in the pathogeneis of most Staphylococcus aureus infections is attachment to biological substrates in vivo using specific protein-protein interactions. We previously quantified the temporal expression of the collagen adhesin (CNA) on S. aureus Phillips and demonstrated that dynamic adhesin capacity to collagen is strongly influenced by the adhesin density.