Vitamin D3 analog maxacalcitol (OCT) induces hCAP-18/LL-37 production in human oral epithelial cells.
Tada. Hiroyuki H; Shimizu. Takamitsu T; Nagaoka. Isao I; Takada. Haruhiko H
Key Findings
- OCT strongly boosts LL‑37 mRNA and protein levels in several oral epithelial cell lines, especially Ca9-22.
- The increase in LL‑37 is dose‑ and time‑dependent, lasting up to 6 days in culture.
- LL‑37 generated by OCT‑treated cells can kill the periodontal pathogen P. gingivalis.
Practical Outcomes
- For biohackers interested in oral health, OCT (or similar vitamin D analogs) could be explored as a way to enhance the mouth's natural antimicrobial defenses. However, the evidence is limited to cell culture, and OCT is not a common supplement, so any real‑world protocol would need careful dosing studies and safety checks before use.
Summary
A synthetic vitamin D3 analog called maxacalcitol (OCT) makes human mouth‑lining cells produce more of the natural antimicrobial peptide LL‑37, which can kill the gum‑disease bug Porphyromonas gingivalis in lab tests.
Abstract
Maxacalcitol (22-oxacalcitriol: OCT) is a synthetic vitamin D3 analog with a limited calcemic effect. In this study, we investigated whether OCT increases the production of LL-37/CAP-18, a human cathelicidin antimicrobial peptide, in human gingival/oral epithelial cells. A human gingival epithelial cell line (Ca9-22) and human oral epithelial cell lines (HSC-2, HSC-3, and HSC-4) exhibited the enhanced expression of LL-37 mRNA upon stimulation with OCT as well as active metabolites of vitamins D3 and D2. Among the human epithelial cell lines, Ca9-22 exhibited the strongest response to these vitamin D-related compounds. OCT induced the higher production of CAP-18 (ng/mL order) until 6 days time-dependently in Ca9-22 cells in culture. The periodontal pathogen Porphyromonas gingivalis was killed by treatment with the LL-37 peptide. These findings suggest that OCT induces the production of hCAP-18/LL-37 in a manner similar to that induced by the active metabolite of vitamin D3.
Study Information
pubmed
2016
2016-06-01T00:00:00.000Z
10.2220/biomedres.37.199
12
31