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Identification of bacterial biofilm and the Staphylococcus aureus derived protease, staphopain, on the skin surface of patients with atopic dermatitis

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by an impaired epidermal barrier, dysregulation of innate and adaptive immunity, and a high susceptibility to bacterial colonization and infection. In the present study, bacterial biofilm was visualized by electron microscop...

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Bibliographic Details
Published in:Scientific reports 2017-08, Vol.7 (1), p.8689-12, Article 8689
Main Authors: Sonesson, Andreas, Przybyszewska, Kornelia, Eriksson, Sigrid, Mörgelin, Matthias, Kjellström, Sven, Davies, Julia, Potempa, Jan, Schmidtchen, Artur
Format: Article
Language:English
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Summary:Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by an impaired epidermal barrier, dysregulation of innate and adaptive immunity, and a high susceptibility to bacterial colonization and infection. In the present study, bacterial biofilm was visualized by electron microscopy at the surface of AD skin. Correspondingly, Staphylococcus aureus ( S . aureus ) isolates from lesional skin of patients with AD, produced a substantial amount of biofilm in vitro . S . aureus biofilms showed less susceptibility to killing by the antimicrobial peptide LL-37 when compared with results obtained using planktonic cells. Confocal microscopy analysis showed that LL-37 binds to the S . aureus biofilms. Immuno-gold staining of S . aureus biofilm of AD skin detected the S . aureus derived protease staphopain adjacent to the bacteria. In vitro , staphopain B degraded LL-37 into shorter peptide fragments. Further, LL-37 significantly inhibited S . aureus biofilm formation, but no such effects were observed for the degradation products. The data presented here provide novel information on staphopains present in S . aureus biofilms in vivo , and illustrate the complex interplay between biofilm and LL-37 in skin of AD patients, possibly leading to a disturbed host defense, which facilitates bacterial persistence.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-017-08046-2