Targeting staphylococcal colonization and virulence

Atopic dermatitis (AD) is a chronic inflammatory skin disorder, affecting 15-20% of children and up to 10% of adults. During disease flares, patients experience inflamed skin lesions accompanied by intense itch. Dysbiosis of the skin’s microbiota occurs where there is a significant reduction in bacterial diversity and higher colonization by staphylococci.

This project will explore staphylococcal adherence to the stratum corneum (SC) of AD skin and the potential to reduce colonization by disrupting adhesion. We recently found that ClfB and FnBPB, cell wall-anchored protein (CWAP) adhesins displayed on the surface of Staphylococcus aureus, recognize the SC protein corneodesmosin and are responsible for the adhesion of S. aureus to AD skin. Unlike S. aureus, there is a paucity of knowledge of the molecular mechanisms used by Staphylococcus epidermidis to adhere to the SC. S. epidermidis produces a smaller number of CWAPs than S. aureus.

This project will deliver a better understanding of the molecular mechanisms used by S. epidermidis to adhere to and colonize the SC in AD. It aims to evaluate, using in vitro models, the performance of selected lead actives for their potential to prevent or disrupt colonization of the SC by S. aureus and S. epidermidis. The effects of formulation on the efficacy of lead actives as decolonization agents will be explored.