Understanding the role of bacterial adhesion during Staphylococcus aureus skin colonisation in atopic dermatitis

特应性皮炎(AD，俗称湿疹)是儿童最常见的慢性皮肤病。金黄色葡萄球菌附着在皮肤表面死亡的扁平细胞上，称为角质细胞，增加炎症并恶化AD症状。我们的研究旨在揭示支持金黄色葡萄球菌附着到角膜细胞的一整套细菌蛋白，并确定它们相互作用的宿主因素。该项目还旨在了解作为共生体存在于皮肤上的其他相关细菌(凝固酶阴性葡萄球菌)如何调节金黄色葡萄球菌在皮肤上的黏附。从这个项目中获得的知识将开启以金黄色葡萄球菌与角膜细胞相互作用为靶点的可能性，作为一种策略，专门干扰金黄色葡萄球菌的粘连，防止或消除AD患者的定植。

Atopic dermatitis (AD, also commonly called eczema), is the most common chronic skin disorder in children. The bacterium Staphylococcus aureus sticks to dead flattened cells on the surface of skin known as corneocytes, increasing inflammation and worsening AD symptoms. Our research aims to uncover the complete set of bacterial proteins that support the attachment of S. aureus to corneocytes and to identify the host factors they interact with. This project also aims to provide an understanding of how other related bacteria that exist on the skin as commensals (coagulase negative staphylococci) regulate the adherence of S. aureus to the skin. The knowledge gained from this project will open up the possibility of targeting S. aureus-corneocyte interactions as a strategy to specifically interfere with S. aureus adhesion and prevent or eliminate colonisation in AD patients.