SKIN CARE 31


Figure 5: Skin illustration shows the process of COL17 shedding in response to oxidative stress by activation of ADAM9 protease and cleavage of dermal- epidermal junction proteins, inc. COL17A and hemidesmosomal proteins


skin. Barrier weakness is not only a surface lipid problem; it is also, in part, a repair problem. When the basal epidermal compartment is less able to maintain renewal and stable anchoring, the skin becomes more fragile and more susceptible to ongoing inflammatory feedback. Literature also indicates that reactive oxygen


species can enhance ADAM9 expression and thereby increase collagen XVII shedding, linking


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oxidative stress directly to structural erosion at the cell surface.8 Figure 5 shows the process of COL17 shedding


in response to oxidative stress by activation of ADAM9 protease and cleavage of dermal- epidermal junction proteins including COL17A and hemidesmosomal proteins. This results in loss of adhesion of basal keratinocytes which subsequently differentiate. The dermal-


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epidermal junction is weakened resulting in age-related structural deterioration of the skin and compromised stem cell niche. Against this backdrop, our 3D in vitro work


suggests that the bisabolol–ginger complex increases COL17A1 at both gene and protein level and is associated with epidermal thickening activity (Figure 6). Interpreted mechanistically, this points to


more than transient comfort. It suggests support for a biological context in which repair, resilience, and barrier quality may improve over time. This is a powerful formulation message because it translates soothing from a short-term sensory benefit into a structural benefit with relevance to well-ageing and chronic reactivity.


Exposome relevance: UV, pollution, and oxidative stress Any state-of-the-art discussion of sensitive skin must also account for the exposome. Skin is continuously challenged by ultraviolet radiation, airborne pollutants, and oxidative stress, all of which contribute to inflammatory signaling, matrix damage, and barrier impairment.4,9–11 For consumers, these stressors are not


Figure 6: A: Bar graphs depict COL17A1 gene expression and B: epidermal thickness. B: EpiDerm reconstituted 3D models (MatTek) were cultivated for 24 hours. The blend was applied for 24 hours. Then EpiDerm models were harvested by fixation using 4% Formaldehyde and embedded in paraffin. Samples were sliced and stained with Hematoxylin/Eosin followed by dehydration, clearing and mounting of the sample. Finally, sections were imaged using a microscope and images were analysed to reveal epidermal thickness


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theoretical. They are part of daily life, especially in urban settings and in routines that include frequent cleansing, shaving, or outdoor exposure. Available literature and our ex vivo and molecular testing together illustrate a clear mechanistic link between pollution, the exposome, and sensitivity biology. Urban particulate matter can drive ROS production through AhR- and NADPH oxidase- related processes, activate downstream kinase and transcription-factor pathways, upregulate


May 2026 PERSONAL CARE MAGAZINE


COL17A1 relative gene expression


Epidermal Thickness (a.u.)


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