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Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin
Published on: July 14, 2017
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Cytokine regulation during epidermal differentiation and barrier formation
Atsunari Tsuchisaka1, Minao Furumura1, Takashi Hashimoto1
1Department of Dermatology, Kurume University School of Medicine, and Kurume University Institute of Cutaneous Cell Biology, Kurume, Japan.
The Journal of Investigative Dermatology
|April 16, 2014
Summary
Atopic dermatitis (AD) involves skin fragility due to Th2 cytokines like IL-4 and IL-13. These cytokines reduce keratin and desmosomal cadherin expression, compromising epidermal integrity and contributing to AD pathogenesis.
Area of Science:
- Dermatology
- Immunology
- Cell Biology
Background:
- The pathophysiology of atopic dermatitis (AD) involves epidermal structural components and cell adhesion.
- The precise role of Th2 cytokines in epidermal instability in AD remains incompletely understood.
Purpose of the Study:
- To investigate the impact of Th2 cytokines on epidermal structural proteins and cell adhesion molecules relevant to atopic dermatitis.
Main Methods:
- Analysis of keratin and desmosomal cadherin expression.
- Investigation of STAT6-dependent signaling pathways.
Main Results:
- Interleukin-4 (IL-4) and Interleukin-13 (IL-13) were found to downregulate keratin and desmosomal cadherin expression.
- This downregulation was dependent on the Signal Transducer and Activator of Transcription 6 (STAT6) pathway.
- The observed changes led to increased keratinocyte fragility under mechanical stress.
Conclusions:
- Th2 cytokine-induced downregulation of structural components contributes to epidermal instability.
- This epidermal instability is a potential pathogenic mechanism in atopic dermatitis.
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