RNA III inhibiting peptide inhibits in vivo biofilm formation by drug-resistant Staphylococcus aureus

Abstract

Staphylococcus aureus is a prevalent cause of bacterial infections associated with indwelling medical devices. RNA III inhibiting peptide (RIP) is known to inhibit S. aureus pathogenesis by disrupting quorum-sensing mechanisms. RIP was tested in the present study for its ability to inhibit S. aureus biofilm formation in a rat Dacron graft model. The activity of RIP was synergistic with those of antibiotics for the complete prevention of drug-resistant S. aureus infections.

FIG. 1.

Proposed mechanism of regulation of cell adhesion and toxin production via TRAP and agr. (A) As the cells multiply, RAP accumulates in the supernatant, binds to its receptor, and induces the phosphorylation of TRAP. Cell adhesion is induced (at the early to midexponential phase of growth), as is the activation of agr (at the midexponential phase of growth). This leads to the production of AIP, which indirectly reduces the level of TRAP phosphorylation, and thus, cell adhesion is repressed (from the midexponential phase of growth). In parallel, RNA III is made, and the RNA III upregulates the production of toxins and the repression of surface proteins (postexponential phase of growth). (B) In the presence of RIP, TRAP is not phosphorylated, agr is not activated, AIP is not made, toxins are not produced, and biofilms do not form.