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Cutaneous Immune Cell-Microbiota Interactions Are Controlled by Epidermal JunB/AP-1
Özge Uluçkan1, Maria Jiménez1, Ben Roediger2
1Cancer Cell Biology Program, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain.
Cell Reports
|October 24, 2019
Summary
This study reveals JunB is crucial for regulating skin immunity and preventing Staphylococcus aureus colonization in atopic dermatitis (AD). Understanding this pathway highlights new therapeutic targets for AD and related skin dysbiosis.
Area of Science:
- Immunology
- Dermatology
- Microbiology
Background:
- Atopic dermatitis (AD) involves complex immune responses, including type 2 and type 17 activation.
- Staphylococcus aureus colonization is common in AD, but mechanisms of dysbiosis and IL-17A's role are unclear.
Purpose of the Study:
- Investigate the role of JunB in AD pathogenesis and Staphylococcus aureus colonization.
- Elucidate the involvement of IL-17A in controlling S. aureus-induced skin inflammation.
Main Methods:
- Utilized JunB mutant mice (JunBΔep) and Rag1 knockout mice to study AD pathology and immune responses.
- Employed prophylactic and therapeutic antibiotic treatments in Il17a-eGFP reporter mice.
- Analyzed keratinocyte function in vitro and in vivo.
Main Results:
- JunBΔep mice exhibited AD-like pathology, including S. aureus colonization, supporting a link between JunB and AD.
- Adaptive immune cells are essential for preventing S. aureus colonization.
- Prophylactic antibiotics reduced IL-17A expression and skin inflammation, unlike post-dysbiosis treatment.
Conclusions:
- JunB acts as a key regulator of host-microbiota interactions in the skin.
- The study characterizes the IL-17A response during spontaneous dysbiosis, offering insights into AD pathogenesis.
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