Exploring the Role of <i>Staphylococcus Aureus</i> Toxins in Atopic Dermatitis
Fabio Seiti Yamada Yoshikawa,
Josenilson Feitosa de Lima,
Maria Notomi Sato,
Yasmin Álefe Leuzzi Ramos,
Valeria Aoki,
Raquel Leao Orfali
Affiliations
Fabio Seiti Yamada Yoshikawa
Laboratory of Dermatology and Immunodeficiencies (LIM-56), Department of Dermatology, University of Sao Paulo Medical School, Sao Paulo-SP 01246-903, Brazil
Josenilson Feitosa de Lima
Laboratory of Dermatology and Immunodeficiencies (LIM-56), Department of Dermatology, University of Sao Paulo Medical School, Sao Paulo-SP 01246-903, Brazil
Maria Notomi Sato
Laboratory of Dermatology and Immunodeficiencies (LIM-56), Department of Dermatology, University of Sao Paulo Medical School, Sao Paulo-SP 01246-903, Brazil
Yasmin Álefe Leuzzi Ramos
Laboratory of Dermatology and Immunodeficiencies (LIM-56), Department of Dermatology, University of Sao Paulo Medical School, Sao Paulo-SP 01246-903, Brazil
Valeria Aoki
Laboratory of Dermatology and Immunodeficiencies (LIM-56), Department of Dermatology, University of Sao Paulo Medical School, Sao Paulo-SP 01246-903, Brazil
Raquel Leao Orfali
Laboratory of Dermatology and Immunodeficiencies (LIM-56), Department of Dermatology, University of Sao Paulo Medical School, Sao Paulo-SP 01246-903, Brazil
Atopic dermatitis (AD) is a chronic and inflammatory skin disease with intense pruritus and xerosis. AD pathogenesis is multifactorial, involving genetic, environmental, and immunological factors, including the participation of Staphylococcus aureus. This bacterium colonizes up to 30−100% of AD skin and its virulence factors are responsible for its pathogenicity and antimicrobial survival. This is a concise review of S. aureus superantigen-activated signaling pathways, highlighting their involvement in AD pathogenesis, with an emphasis on skin barrier disruption, innate and adaptive immunity dysfunction, and microbiome alterations. A better understanding of the combined mechanisms of AD pathogenesis may enhance the development of future targeted therapies for this complex disease.
