Clumping factor B promotes adherence of Staphylococcus aureus to corneocytes in atopic dermatitis

Staphylococcus aureus skin infection is a frequent and recurrent problem in children with the common inflammatory skin disease atopic dermatitis (AD). S. aureus colonises the skin of the majority of children with AD and exacerbates the disease. The first step during colonisation and infection is bacterial adhesion to the cornified envelope of corneocytes in the outer layer stratum corneum. Corneocytes from AD skin are structurally different to corneocytes from normal healthy skin. The objective of this study was to identify bacterial proteins that promote the adherence of S. aureus to AD corneocytes. S. aureus strains from clonal complex 1 and 8 were more frequently isolated from infected AD skin than from the nasal cavity of healthy children. AD strains had increased ClfB ligand binding activity compared to normal nasal carriage strains. Adherence of single S. aureus bacteria to corneocytes from AD patients ex vivo was studied using atomic force microscopy. Bacteria expressing ClfB recognised ligands distributed over the entire corneocyte surface. The ability of an isogenic ClfB-deficient mutant to adhere to AD corneocytes was greatly reduced compared to its parent clonal complex 1 clinical strain. ClfB from clonal complex 1 strains had a slightly higher binding affinity for its ligand compared to ClfB from other clonal complexes. Our results provide new insights into the first step in the establishment of S. aureus colonisation in AD patients. ClfB is a key adhesion molecule for the interaction of S.aureus with AD corneocytes and represents a target for intervention.