Mary Turley’s research is focused on elucidating the molecular mechanisms underpinning how Staphylococcus aureus colonises the host and establishes invasive infection. Key areas of her experience include:
Molecular mechanisms underpinning skin colonisation. Staphylococcus aureus predominance is significantly associated with severe Atopic dermatitis, a chronic inflammatory skin condition. Cell wall anchored proteins displayed on the surface of S. aureus facilitate this colonisation and recent work from the Geoghegan lab has distinguished the contribution two specific cell wall proteins have to this interaction. Mary’s postdoctoral work aims to provide a comprehensive understanding of the complete repertoire of adhesive interactions occurring during S. aureus skin colonisation in atopic dermatitis and to uncover how commensal staphylococci impede the adhesion of S. aureus to healthy skin.
Mechanics of Staphylococcus aureus biofilm formation. S. aureus is one of the pathogens most frequently isolated from the airways of cystic fibrosis patients. Bile is frequently aspirated into the lungs of these patients, often because of gastroesophageal reflux. Mary’s work details the microbial genomic and regulatory response to bile exposure and its implications for anti-biofilm treatment. This research provides new insight into how S. aureus may adopt its persistent lifestyle in the cystic fibrosis airways and enhances knowledge of host-pathogen interactions, biofilm formation and antibiotic resistance.
Proteolytic processing of Staphylococcal adhesins. Clumping factor A (ClfA) is a staphylococcal fibrinogen-binding cell wall-anchored protein that serves as a key virulence factor during invasive infection, promoting bloodstream survival. My work below investigated the impact of the proteolytic processing of host endopeptidase Plasmin on ClfA and determined how it influenced staphylococcal aggregation and abscess formation. This work contributes crucial knowledge on host protease activity, protein-protein interactions, and staphylococcal virulence during systemic infection.