Figure 1. Injury triggers increased TLR2, CD14, and CYP24A1 in skin.

Human wounds 24 hours after full-thickness sterile skin incision were evaluated for the expression of innate immune recognition and response molecules (n = 5). Transcript abundance was measured by qPCR, normalized to GAPDH expression, and compared with noninjured skin (n = 4). (A) Wounded skin showed an expected increase in expression of cathelicidin, a vitamin D₃–responsive antimicrobial gene. Additional vitamin D₃–responsive genes, the TLR co-receptor CD14 (B) and the vitamin D₃ catabolic enzyme CYP24A1 (C), also increased after injury. (D) Expression of TLR2 mRNA, but not that of TLR1, TLR4, and TLR6, was increased after injury. (E) A corresponding increase in TLR2 protein staining on keratinocytes at the wound edges was seen (original magnification, ×100). The incision site is marked by black arrows. An enlarged sector is displayed in the inset (original magnification, ×400). *P < 0.05, Mann-Whitney test.