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Staphylococcus aureus-derived membrane vesicles exacerbate skin inflammation in atopic dermatitis
1Department of Microbiology, Kyungpook National University School of Medicine, Daegu, Korea.
Background:
Skin colonization or infection with Staphylococcus aureus is known to trigger aggravation of atopic dermatitis (AD). However, the exact mechanisms by which S. aureus can worsen AD are unknown.
Objective:
We investigated whether and how S. aureus-derived membrane vesicles (MVs) contribute to worsening of AD.
Methods:
Immunohistochemical and immunoelectron microscopic analyses were performed to detect staphylococcal protein A (SPA) in the epidermis of AD lesions. HaCaT cells were treated with S. aureus MVs and were analysed for the expression of cytokine genes. Immunopathology and cytokine gene profiles were analysed after topical application of S. aureus MVs to AD-like skin lesions in a mouse model.
Results:
The MV component SPA was detected in the keratinocytes as well as in the intercellular space of the epidermis of AD lesions colonized with S. aureus. Intact MVs from S. aureus delivered their components to keratinocytes and stimulated pro-inflammatory cytokine gene expression in vitro. A knock-down of Toll-like receptor 2 or nucleotide-binding oligomerization domain 2 using small interfering RNAs suppressed interleukin-8 gene expression. Topical application of intact S. aureus MVs to AD-like skin lesions in the mouse model induced massive infiltration of inflammatory cells and the resulting eczematous dermatitis. This inflammatory reaction was associated with a mixed Th1/Th2 immune response and enhanced expression of chemokine genes in AD-like skin lesions.
Conclusions And Clinical Relevance:
This study showed the importance of S. aureus MVs as a potent mediator for worsening of AD among many exogenous worsening factors of AD. Thus, S. aureus MVs may be regarded as one of the therapeutic targets for the management of AD aggravation.
Insights
Staphylococcus aureus membrane vesicles (MVs) worsen atopic dermatitis (AD) by delivering components like staphylococcal protein A (SPA) to skin cells, triggering inflammation. These MVs are a potential therapeutic target for managing AD aggravation.
Area of Science:
- Dermatology
- Microbiology
- Immunology
Background:
- Atopic dermatitis (AD) severity is linked to Staphylococcus aureus colonization.
- The precise mechanisms by which S. aureus exacerbates AD remain unclear.
Purpose of the Study:
- To investigate the role of S. aureus-derived membrane vesicles (MVs) in worsening atopic dermatitis.
- To elucidate the molecular mechanisms underlying S. aureus MV-induced AD aggravation.
Main Methods:
- Detection of staphylococcal protein A (SPA) in AD skin lesions using immunohistochemistry and immunoelectron microscopy.
- In vitro analysis of keratinocyte response to S. aureus MVs, including cytokine gene expression.
- In vivo assessment of S. aureus MV effects on AD-like skin lesions in a mouse model.
Main Results:
- SPA, an MV component, was found in the epidermis of S. aureus-colonized AD lesions.
- S. aureus MVs stimulated pro-inflammatory cytokine and chemokine gene expression in keratinocytes.
- Topical application of S. aureus MVs induced significant inflammation and eczematous dermatitis in a mouse model, associated with a Th1/Th2 immune response.
Conclusions:
- S. aureus MVs are significant mediators contributing to the worsening of atopic dermatitis.
- S. aureus MVs represent a potential therapeutic target for mitigating AD aggravation.
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