Injury-induced innate immune response in human skin mediated by transactivation of the epidermal growth factor receptor
Ole E. Sørensen, … , Artur Schmidtchen, Tomas Ganz
Ole E. Sørensen, … , Artur Schmidtchen, Tomas Ganz
Published July 3, 2006
Citation Information: J Clin Invest. 2006;116(7):1878-1885. https://doi.org/10.1172/JCI28422.
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Research Article Dermatology

Injury-induced innate immune response in human skin mediated by transactivation of the epidermal growth factor receptor

Abstract

We found that sterile wounding of human skin induced epidermal expression of the antimicrobial (poly)peptides human β-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 β-defensin–3 and increased the activity of organotypic epidermal cultures against Staphylococcus aureus. These data demonstrate that sterile wounding initiates an innate immune response that increases resistance to overt infection and microbial colonization.

Authors

Ole E. Sørensen, Dharma R. Thapa, K. Markus Roupé, Erika V. Valore, Ulf Sjöbring, Alice A. Roberts, Artur Schmidtchen, Tomas Ganz

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Figure 6

The expression of EGFR and EGFR ligands in wounded skin.

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The expression of EGFR and EGFR ligands in wounded skin. The expression ...
The expression of mRNA of EGFR, TGF-α, HB-EGF, amphiregulin, and hBD-3 was analyzed by real-time qRT-PCR. The mRNA expression is shown as the difference in threshold cycles between the gene of interest and G3PD. The expression of EGFR and its ligands was stable over time.