Inflammatory skin diseases, such as psoriasis and atopic dermatitis, represent complex, multifactorial conditions driven by dysregulated immune responses and intricate cellular interactions, posing significant challenges for therapeutic development. Protheragen provides specialized skin-on-a-chip (SoC) model development services specifically engineered to recapitulate the pathophysiology of inflammatory skin diseases. We create sophisticated, microfluidic-based in vitro platforms, offering a high biological fidelity system for studying disease mechanisms and screening potential interventions.
Applications of Inflammatory Skin-on-a-Chip Models
Physiologically relevant skin-on-a-chip models serve as powerful tools for both basic research and preclinical drug development, enabling detailed investigation into inflammatory processes in a controlled, human-mimetic environment. These microfluidic systems encapsulate primary or patient-derived human keratinocytes and fibroblasts, as well as immune cells in a 3D, perfused microenvironment, where critical features of inflamed skin, including vascularization, immune cell trafficking and recruitment, and cytokine gradients are simulated.
Disease Mechanistic Studies
Investigate the intricate interplay between immune cells (e.g., T cells, macrophages), cytokines (e.g., TNF-α, IL-17), and resident skin cells driving inflammation and barrier dysfunction.
Drug Screening and Efficacy Testing
Evaluate the therapeutic potential and mechanism of action of novel compounds, biologics, and topical formulations in a high-throughput, physiologically relevant setting, providing robust data for lead optimization.
Case Study: Inflammatory Skin-on-a-Chip Model Development
In response to the need for physiologically relevant models for human inflammatory skin disease, we developed and validated a TNF-α-induced inflammatory skin-on-a-chip model. This microfluidic system integrated epidermal, dermal, and vascular layers to simulate human skin structure while capturing essential cellular interactions and inflammatory pathways for enhanced therapeutic screening.

Fig.1 TNF-α induction significantly increased proinflammatory cytokines, which were then reduced by drug therapy.
Exposure to 60 ng/ml TNF-α induced a strong inflammatory response, marked by increased levels of IL-1β, IL-6, and IL-8. The model was subsequently utilized to evaluate a drug, which significantly reduced the release of these inflammatory mediators. The system effectively captured both the onset of inflammation and its resolution following drug treatment, demonstrating its practical utility.
Related Services
In addition to our skin-on-a-chip platforms, we provide comprehensive in vitro and in vivo model development services to assist your research at all stages. Our expertise extends to developing cell-based and organoid models for high-throughput screening and designing and conducting in vivo studies in appropriate animal models of inflammatory skin disease.
With Protheragen’s in-depth expertise, knowledge, and skin biology and engineering expertise, along with our highly predictive and customizable models, we can offer an integrated solution from design and development to data analysis and reporting to support your preclinical studies in pharmacodynamics, pharmacokinetics, and toxicology. For more information on our inflammatory skin-on-a-chip model development services, empowering your research and accelerating your drug development programs, please reach out to us.
References
- Kim, Kyunghee et al. “An Interleukin-4 and Interleukin-13 Induced Atopic Dermatitis Human Skin Equivalent Model by a Skin-On-A-Chip.” International journal of molecular sciences 23.4 (2022): 2116.
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only and cannot be used to diagnose, treat or manage patients.