The effect of calcipotriol on the expression of human beta defensin-2 and LL-37 in cultured human keratinocytes.
Kim. Beom Joon BJ; Rho. Yong Kwan YK; Lee. Hye In HI; Jeong. Mi Sook MS; Li. Kapsok K; Seo. Seong Jun SJ; Kim. Myeung Nam MN; Hong. Chang Kwun CK
Key Findings
- Inflammatory triggers like LPS, UVB, and TNF‑alpha raise LL‑37 and HBD‑2 in cultured human keratinocytes
- Calcipotriol treatment reduces the elevated LL‑37 and HBD‑2 back toward baseline
- The experiments were done in vitro using PCR, Western blot and staining techniques
Practical Outcomes
- If you use calcipotriol (e.g., for psoriasis) you might unintentionally suppress LL‑37, potentially weakening skin antimicrobial protection. For biohackers aiming to boost LL‑37, avoid topical calcipotriol or consider timing it away from periods when you want high peptide levels. The finding is mainly confirmatory and not a new protocol.
Summary
The study shows that a skin‑applied vitamin D drug called calcipotriol can lower the levels of the antimicrobial peptide LL‑37 (and beta‑defensin‑2) that are normally boosted by inflammation or UV light in skin cells. This means using calcipotriol may dampen a part of the skin’s natural immune defense.
Abstract
Vitamin D has been reported to regulate innate immunity by controlling the expression of antimicrobial peptides (AMPs). We investigated the effect of calcipotriol on the expression of AMPs in human cultured keratinocytes. Keratinocytes were treated with lipopolysaccharide (LPS), TNF-alpha, Calcipotriol and irradiated with UVB, cultured, and harvested. To assess the expression of human beta defensin-2 and LL-37 in the control group, not exposed to any stimulants, the experimental group was treated with LPS, TNF-alpha, or UVB, and another group was treated again with calcipotriol; reverse transcriptase-polymerase chain reaction, Western blotting, and immunohistochemical staining were performed. In the experimental group treated with LPS, UVB irradiation, and TNF-alpha, the expression of beta-defensin and LL-37 was increased more than in the control group and then decreased in the experimental group treated with calcipotriol. Calcipotriol suppressed HBD-2 and LL-37, which were stimulated by UVB, LPS, and TNF-alpha.
Study Information
pubmed
2010
2010-02-22T00:00:00.000Z
10.1155/2009/645898
43
29