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Clumping Factor B Promotes Adherence of Staphylococcus aureus to Corneocytes in Atopic Dermatitis
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.
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“ClfB-deficient mutants show reduced bacterial burden and milder pathology in skin abscess models, indicating its importance in disease progression.”
From Staphylococcus aureus: A Review of the Pathogenesis and Virulence Mechanisms (2025) · cites this paper as [47]
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“Studies have shown that ClfB-deficient strains exhibit reduced binding to human corneocytes, highlighting its importance in colonization [47].”
From Staphylococcus aureus: A Review of the Pathogenesis and Virulence Mechanisms (2025) · cites this paper as [47]
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Self-citationWILLIAMS, H. C., JBURNEY, P. G., HAY, R. J., ARCHER, C. B., SHIPLEY, M. J., AHUNTER, J. J., BINGHAM, E. A., FINLAY, A. Y., PEMBROKE, A. C., CGRAHAM-BROWN, R. A., et al. (1994) · British Journal of Dermatology · doi:10.1111/j.1365-2133.1994.tb08530.x · Cited by 1,271
Filaggrin Mutations Associated with Skin and Allergic Diseases
Irvine, A. D., McLean, W. H. I., & Leung, D. Y. M. (2011) · New England Journal of Medicine · doi:10.1056/nejmra1011040 · Cited by 1,217
Self-citationStaphylococcus δ-toxin induces allergic skin disease by activating mast cells
Nakamura, Y., Oscherwitz, J., Cease, K. B., Chan, S. M., Muñoz-Planillo, R., Hasegawa, M., Villaruz, A. E., Cheung, G. Y. C., McGavin, M. J., Travers, J. B., et al. (2013) · Nature · doi:10.1038/nature12655 · Cited by 558
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The microbiome in patients with atopic dermatitis
Paller, A. S., Kong, H. H., Seed, P., Naik, S., Scharschmidt, T. C., Gallo, R. L., Luger, T., & Irvine, A. D. (2019) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2018.11.015 · Cited by 525
Self-citationStaphylococcus aureus: A Review of the Pathogenesis and Virulence Mechanisms
Touaitia, R., Mairi, A., Ibrahim, N. A., Basher, N. S., Idres, T., & Touati, A. (2025) · Antibiotics · doi:10.3390/antibiotics14050470 · Cited by 273
The exposome in atopic dermatitis
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Self-citationPrebiotics in atopic dermatitis prevention and management
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Metadata
- Authors
- Fleury, O. M., McAleer, M. A., Feuillie, C., Formosa-Dague, C., Sansevere, E., Bennett, D. E., Towell, A. M., McLean, W. H. I., Kezic, S., Robinson, D. A., Fallon, P. G., Foster, T. J., Dufrêne, Y. F., Irvine, A. D., & Geoghegan, J. A.
- Affiliations
- Department of Microbiology, Moyne Institute of Preventive Medicine, School of Genetics and Microbiology, Trinity College Dublin, Dublin, Ireland
- Clinical Medicine, Trinity College Dublin, Dublin, Ireland
- Institute of Life Sciences, Université Catholique de Louvain, Louvain-la-Neuve, Belgium
- Department of Microbiology and Immunology, University of Mississippi Medical Center, Jackson, Mississippi, USA
- Epidemiology and Molecular Biology Unit, Temple Street Children's University Hospital, Dublin, Ireland
- Dermatology and Genetic Medicine, University of Dundee, Dundee, United Kingdom
- Coronel Institute of Occupational Health, Academic Medical Center, Amsterdam, The Netherlands
- Venue
- Infection and Immunity
- Publisher
- American Society for Microbiology
- Published
- 2017-06
- Volume
- 85
- Issue
- 6
- ISSN
- 0019-9567
- 1098-5522
- Cited by
- 100
- References
- 4
- Language
- en
- Licence
- journals.asm.org/non-commercial-tdm-license (tdm)
- Funders
- National Children's Research Centre, Dublin Ireland
- Wellcome Trust (092530/Z/10/Z)
- National Fund for Scientific Research (WELBIO-CR-2015A-05)
- NIH (GM080602)
- European Research Council (693630)
- British Skin Foundation
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- CoChat. (2026). Citation check: Clumping Factor B Promotes Adherence of Staphylococcus aureus to Corneocytes in Atopic Dermatitis. https://app.cochat.ai/papers/10.1128/iai.00994-16
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- Fleury, O. M., McAleer, M. A., Feuillie, C., Formosa-Dague, C., Sansevere, E., Bennett, D. E., Towell, A. M., McLean, W. H. I., Kezic, S., Robinson, D. A., Fallon, P. G., Foster, T. J., Dufrêne, Y. F., Irvine, A. D., & Geoghegan, J. A. (2017). Clumping Factor B Promotes Adherence of Staphylococcus aureus to Corneocytes in Atopic Dermatitis. Infection and Immunity. https://doi.org/10.1128/iai.00994-16
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
