Device-related infections caused by S. epidermidis through its ability to form biofilms are of serious medical concern. Colonisation and development of biofilms by this opportunistic pathogen is favoured on the surfaces of biomaterial insertions, such as central venous catheters, coronary stents and orthopedic implants. S. epidermidis infections particularly affect immunocompromised patients, and those with surgical implants. In a biofilm, S. epidermidis is protected from the host immune system, and are resistant to antibiotics due to the encapsulation within the biofilm matrix. This makes device-related infections caused by S. epidermidis difficult to treat and eradicate. In S. epidermidis, biofilm formation is mediated by PIA (the major intercellular adhesin), the foundation for biofilm formation. A novel and enigmatic adpS (autoinducer degrading protein of Staphylococcus) gene was identified in a biofilm-negative variant in James P. O’Gara’s lab. Using a clinical S. epidermidis strain CSF41498 isolated from a patient in Beaumont Hospital with a neurosurgical device-related infection, research in the lab demonstrated that overexpression of adpS on a multicopy plasmid was associated with increased biofilm formation. To further investigate the mechanism of AdpS-mediated biofilm regulation, by way of a combined Bacterial Two Hybrid system and genomic DNA library screening approach, this project aims to identify potential protein interaction partners of AdpS. The protein-protein interactions identified throughout this project will provide a basis for future works to assign a more accurate function to this cryptic gene, with the hope of providing insight for therapeutic interventions to tackle biofilm-originated, antibiotic resistant and chronic infections.
