Injury-induced innate immune response in human skin mediated by transactivation of the epidermal growth factor receptor
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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 Staphylococcus 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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In inflamed skin, including psoriasis and skin injury, hBD3 is inducible by skin injury.
“In inflamed skin, including psoriasis and skin injury, hBD3, which like hBD2 was originally purified from psoriatic skin, is inducible by skin injury.38”
From The Innate Immune System in Acute and Chronic Wounds (2016) · cites this paper as [38]
AMPs can amplify the proinflammatory cytokine response and can thus, in some circumstances, assume pathogenic roles as in psoriasis, rosacea, and other skin diseases.
“AMPs can amplify the proinflammatory cytokine response and can thus, in some circumstances, assume pathogenic roles as in psoriasis, rosacea, and other skin diseases.36–38”
From The Innate Immune System in Acute and Chronic Wounds (2016) · cites this paper as [38]
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References 44 · Cited by 152
- Authors
- Sorensen, O. E.
- Venue
- Journal of Clinical Investigation
- Published
- 2006-07-03
- Volume
- 116
- Issue
- 7
- Pages
- 1878-1885
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC1479426
- OpenAlex
- W1990005751
- Cited by
- 152
- References
- 44
- Citations by year
- 2026: 4 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 5 · 2021: 9 · 2020: 1 · 2019: 3 · 2018: 6 · 2017: 8 · 2016: 10 · 2015: 13 · 2014: 7 · 2013: 8 · 2012: 11
- FWCI
- 13.54
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Funders
- Lunds Universitet
- Novo Nordisk
- Alfred Österlunds Stiftelse
- Alfred Benzon Foundation
- Novo Nordisk Fonden
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL046809, HL46809)
- Topics
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Life Sciences › Immunology and Microbiology › Microbiology › Antimicrobial Peptides and Activities
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Keywords
- epidermal growth factor receptor, skin damage, innate immunity, human beta-defensin 3, neutrophil gelatinase-associated lipocalin, secretory leukocyte protease inhibitor, heparin-binding EGF, metalloproteinases, antimicrobial peptides, Staphylococcus aureus, skin colonization
- MeSH terms
- Lipocalin-2, Acute-Phase Proteins, Animals, Cells, Cultured, Epidermal Growth Factor, Humans, Immunity, Innate, Proteins, Proto-Oncogene Proteins, Skin, Transcriptional Activation, Keratinocytes, Transforming Growth Factor alpha, beta-Defensins, Antimicrobial Cationic Peptides, Mice, Proteinase Inhibitory Proteins, Secretory, Lipocalins, ErbB Receptors
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