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Staphylococcus aureus second immunoglobulin-binding protein drives atopic dermatitis via IL-33
Arwa Al Kindi1, Helen Williams1, Kenshiro Matsuda2
1Lydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester, United Kingdom.
The Journal of Allergy and Clinical Immunology
|October 4, 2020
Summary
Staphylococcus aureus
Area of Science:
- Immunology
- Microbiology
- Dermatology
Background:
- Atopic dermatitis (AD) is frequently triggered by Staphylococcus aureus.
- The mechanism by which S. aureus drives type 2 allergic responses in AD, without infection, remains unclear.
Purpose of the Study:
- Identify the specific S. aureus virulence factor responsible for initiating the cutaneous type 2 immune response in AD.
- Elucidate the role of this factor in the pathogenesis of atopic dermatitis.
Main Methods:
- Utilized in vitro human keratinocyte cultures, ex vivo human skin explants, and a mouse model of eczema.
- Employed fast protein liquid chromatography and mass spectrometry for factor identification.
- Confirmed bioactivity using bacterial expression systems and S. aureus mutant strains.
Main Results:
- S. aureus uniquely induces IL-33 release from keratinocytes, independent of Toll-like receptor pathways.
- Identified S. aureus second immunoglobulin-binding protein (Sbi) as the key virulence factor driving IL-33 release.
- Observed disruption of corneodesmosin and impaired skin barrier function in the mouse model.
Conclusions:
- S. aureus-derived Sbi is a novel virulence factor that promotes type 2 immunity.
- Sbi initiates the type 2 cytokine activity underlying atopic dermatitis pathogenesis.
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