A majority of clinical isolates of skin associated S. aureus were found to lack the gene required to express the collagen binding adhesin (cna). This extends to strains isolated from patients with atopic dermatitis (AD). While S. aureus is found in ~5% of healthy skin, this increases to 50-70% in AD skin. We are funded by the National Eczema Association to uncover the mechanisms that determine the success of S. aureus on AD skin and determine the potential role of inflammation driven by bacterial collagen-binding dynamics.

We will investigate the temporal integration of hECM proteins in microcolony formation, utilizing spatial transcriptomics to map the expression of specific adhesins and detect local hECM signatures within founding bacterial communities. These studies will probe the hierarchy by which S. aureus adhesins recruit, bind, and structurally repurpose matrix components.