Abstract
AbstractInflammation of the skin is not only a key pathological factor of multiple major skin diseases, but also a hallmark of the pathological state of the skin. However, there has been significant deficiency in the biomarkers and approaches for non-invasive evaluations of local inflammation of the skin. In our current study, we used a mouse model of skin inflammation to test our hypothesis that the inflammation of the skin can lead to increased epidermal green autofluorescence (AF), which can become a novel biomarker for non-invasive evaluations of the local inflammation of the skin. We found that 12-O-tetradecanoylphorbol-13-acetate (TPA), a widely used inducer of skin inflammation, induced not only inflammation of the skin, but also increased green AF of the skin. The distinct polyhedral structure of the increased AF has indicated that the AF originates from the keratin 1 and/or keratin 10 of the suprabasal keratinocytes. Our Western blot assays showed that TPA produced dose-dependent decreases in the levels of both keratin 1 and keratin 10, suggesting that TPA produced the increased epidermal green AF at least partially by inducing cleavage of keratin 1 and/or keratin 10. Collectively, our study has indicated that epidermal green AF is a novel biomarker for non-invasive evaluations of the local inflammation of the skin. This finding is of profound and extensive significance for non-invasive and efficient diagnosis of multiple inflammation-mediated skin diseases. This biomarker may also be used for non-invasive and rapid evaluations of the health state of the skin.
Publisher
Cold Spring Harbor Laboratory