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Clumping Factor B Promotes Adherence of Staphylococcus aureus to Corneocytes in Atopic Dermatitis
Orla M Fleury1, Maeve A McAleer2,3,4, Cécile Feuillie5
1Department of Microbiology, Moyne Institute of Preventive Medicine, School of Genetics and Microbiology, Trinity College Dublin, Dublin, Ireland.
Insights
Staphylococcus aureus (S. aureus) adhesion to skin in atopic dermatitis (AD) is promoted by the bacterial protein ClfB. This molecule binds to corneocytes, facilitating S. aureus colonization and exacerbating AD symptoms.
Area of Science:
- Microbiology
- Dermatology
- Infectious Diseases
Background:
- Atopic dermatitis (AD) is frequently complicated by recurrent Staphylococcus aureus (S. aureus) skin infections.
- S. aureus colonization of the skin is common in children with AD and worsens the condition.
- Bacterial adhesion to corneocytes in the stratum corneum is the initial step in S. aureus colonization and infection.
Purpose of the Study:
- To identify bacterial proteins responsible for S. aureus adherence to corneocytes from AD skin.
- To investigate the role of ClfB in the interaction between S. aureus and AD corneocytes.
Main Methods:
- Comparison of S. aureus strains from AD skin and healthy nasal cavities.
- Assessment of ClfB ligand binding activity.
- Atomic force microscopy to study bacterial adherence to ex vivo AD corneocytes.
- Evaluation of a ClfB-deficient mutant's adherence.
Main Results:
- S. aureus strains from clonal complexes 1 and 8 were more prevalent in infected AD skin.
- AD strains exhibited increased ClfB ligand binding activity.
- ClfB-expressing bacteria adhered to AD corneocytes, while ClfB-deficient mutants showed significantly reduced adherence.
- ClfB from clonal complex 1 strains displayed higher binding affinity.
Conclusions:
- ClfB is a crucial adhesion molecule mediating S. aureus interaction with AD corneocytes.
- ClfB plays a key role in the initial colonization of S. aureus in atopic dermatitis.
- ClfB represents a potential therapeutic target for managing S. aureus colonization in AD patients.
Abstract:
Staphylococcus aureus skin infection is a frequent and recurrent problem in children with the common inflammatory skin disease atopic dermatitis (AD). S. aureus colonizes the skin of the majority of children with AD and exacerbates the disease. The first step during colonization and infection is bacterial adhesion to the cornified envelope of corneocytes in the outer layer, the stratum corneum. Corneocytes from AD skin are structurally different from 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 complexes 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 recognized ligands distributed over the entire corneocyte surface. The ability of an isogenic ClfB-deficient mutant to adhere to AD corneocytes compared to that of its parent clonal complex 1 clinical strain was greatly reduced. ClfB from clonal complex 1 strains had a slightly higher binding affinity for its ligand than ClfB from strains from other clonal complexes. Our results provide new insights into the first step in the establishment of S. aureus colonization in AD patients. ClfB is a key adhesion molecule for the interaction of S. aureus with AD corneocytes and represents a target for intervention.