INJURY-INDUCED INNATE IMMUNE RESPONSE IN HUMAN SKIN MEDIATED BY TRANSACTIVATION OF THE EPIDERMAL GROWTH FACTOR RECEPTOR.
This study by researchers at the UCLA School of Medicine (USA) and Lund University (Sweden) demonstrated that sterile wounding of MatTek’s EpiDerm human skin tissue equivalent initiates an in vivo-like innate immune response that increases resistance to overt infection and microbial colonization. Researchers found that sterile wounding of human skin induced epidermal expression of the antimicrobial (poly)peptides human beta-defensin-3, neutrophil gelatinase-associated lipocalin, and secretory leukocyte protease inhibitor through activation of the epidermal growth factor receptor. After skin wounding, the receptor was activated by heparin-binding epidermal growth factor that was released by a metalloprotease-dependent mechanism. Activation of the epidermal growth factor receptor generated antimicrobial concentrations of human â-defensin-3 and increased the activity of the EpiDerm organotypic epidermal cultures against Staphylococcus aureus. These data demonstrate that sterile wounding of EpiDerm organotypic epidermal cultures initiates an innate immune response that increases resistance to overt infection and microbial colonization.
Anti-microbial, Anti-microbial (poly)peptides, Antimicrobial, Antimicrobial (poly)peptides, EpiDerm, Epidermal expression, Epidermal growth factor receptor, Heparin-binding epidermal growth factor, Human beta-defensin-3, Innate immune response, Metalloprotease-dependent, Microbial colonization, Neutrophil gelatinase-associated lipocalin, Organotypic epidermal cultures, Secretory leukocyte protease inhibitor, Skin wounding, Staphylococcus aureus, Sterile wounding
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