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Updated understanding of Staphylococcus aureus in atopic dermatitis: From virulence factors to commensals and clonal complexes
Author(s) -
Hwang Jonwei,
Thompson Alyssa,
Jaros Joanna,
Blackcloud Paul,
Hsiao Jennifer,
Shi Vivian Y.
Publication year - 2021
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.14435
Subject(s) - atopic dermatitis , microbiome , dysbiosis , virulence , staphylococcus aureus , immunology , superantigen , biology , commensalism , microbiology and biotechnology , immune system , genetics , gene , bacteria , t cell
Atopic dermatitis (AD) is a common inflammatory dermatosis that has multiple contributing factors including genetic, immunologic and environmental. Staphylococcus aureus (SA) has long been associated with exacerbation of AD. SA produces many virulence factors that interact with the human skin and immune system. These superantigens and toxins have been shown to contribute to adhesion, inflammation and skin barrier destruction. Recent advances in genome sequencing techniques have led to a broadened understanding of the multiple ways SA interacts with the cutaneous environment in AD hosts. For example, temporal shifts in the microbiome, specifically in clonal complexes of SA, have been identified during AD flares and remission. Herein, we review mechanisms of interaction between the cutaneous microbiome and SA and highlight known differences in SA clonal complexes that contribute to AD pathogenesis. Detailed knowledge of the genetic strains of SA and cutaneous dysbiosis is becoming increasingly relevant in paving the way for microbiome‐modulating and precision therapies for AD.