期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 116, 期 7, 页码 1878-1885出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI28422
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资金
- NHLBI NIH HHS [HL 46809, R01 HL046809] Funding Source: Medline
We 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 beta-defensin-3 and increased the activity of organotypic epidermal cultures against Stapbylococcus aureus. These data demonstrate that sterile wounding initiates an innate immune response that increases resistance to overt infection and microbial colonization.
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