Host defence peptides in human burns.
Kaus. Aljoscha A; Jacobsen. Frank F; Sorkin. Michael M; Rittig. Andrea A; Voss. Bruno B; Daigeler. Adrien A; Sudhoff. Holger H; Steinau. Hans-Ulrich HU; Steinstraesser. Lars L
Key Findings
- Burned skin (especially partial‑thickness burns) shows higher mRNA levels of LL‑37, hBD2, hBD3 and other host‑defence peptides than unburned skin.
- In‑situ hybridisation shows LL‑37, hBD2 and hBD3 are expressed at the surface of burns regardless of how deep the burn is.
- Higher expression of these peptides does not correlate with a lower rate of wound infection in burn patients.
Practical Outcomes
- For DIY health enthusiasts, this research doesn’t provide a new protocol or dosage for LL‑37 supplementation. It mainly confirms that the body naturally ramps up certain antimicrobial peptides after skin injury, but that boost alone isn’t enough to stop infections. Therefore, relying on topical LL‑37 or similar peptides for wound care or systemic health benefits remains unproven.
Summary
The study looked at how the body’s natural antimicrobial peptide LL‑37 (and a few other skin peptides) is produced in burned skin compared to normal skin. They found that burned skin makes more of these peptides, but this increase didn’t seem to prevent infections, suggesting the skin’s innate immune response is complicated.
Abstract
The goal of this study was to analyse expression profiles of human epithelial host defence peptides in burned and unburned skin tissue, samples of which were obtained during debridements and snap-frozen in liquid nitrogen. Total RNA was isolated, and cDNA of epithelial host defence peptides and proteins (hCAP-18/LL-37, hBD1-hBD4, dermcidin, S100A7/psoriasin and RNAse7) was quantified by qRT-PCR. In situ hybridisation and immunohistochemical staining localised gene expression of hCAP-18/LL-37, hBD2 and hBD3 in histological sections. Most of the analysed host defence peptides and proteins showed higher mRNA levels in partial-thickness burns than in unburned tissue. In situ hybridisation revealed expression of hCAP-18/LL-37, hBD2 and hBD3 at the surface of burns that was independent of burn depth. However, the finding of higher host defence peptide gene expression rates does not correlate with the incidence of wound infection in burns. We hypothesise that the epithelial innate immune response in burns is complex.
Study Information
pubmed
2007
2007-08-21T00:00:00.000Z
10.1016/j.burns.2007.04.017