The study shows that vitamin D (calcitriol) can lower certain inflammation markers in blood vessel cells, but it doesn’t change the levels of the antimicrobial peptide LL‑37 or genes linked to new blood‑vessel growth. This suggests vitamin D might help keep blood vessels from getting inflamed, though the work was done in a lab dish, not in people.

Calcitriol (vitamin D) supplementation has been proposed for therapeutical use in vascular diseases due to its immunomodulatory activity, preventing inflammation and promoting angiogenesis. In the present study, we hypothesised whether calcitriol downregulates pro-inflammatory gene expression without affecting angiogenesis and anti-inflammatory gene expression in LPS-induced endothelial cells. In order to evaluate the effect of calcitriol in suppressing inflammatory gene expression in the endothelium, endothelial cells were exposed to the physiological concentration of calcitriol followed by stimulation with lipopolysaccharide (LPS). Gene expression of interleukin (IL)-1β, Transforming Growth Factor (TGF)-β, Human β-defensin (HBD)-2, angiogenin (ANG) and cathelicidin (LL-37) were quantified by quantitative polymerase chain reaction. The results from six independent experiments conducted in duplicate, showed that calcitriol decreased IL-1β (p < 0.01) and HBD-2 expression (p < 0.01) when compared to non-treated cells. However, calcitriol treatment had no effect on TGF-β, ANG and LL-37 gene expression. Calcitriol prevents inflammatory gene expression, but does not affect expression of angiogenic genes in endothelial cells, which suggest the potential use of calcitriol to prevent endothelial activation through the downregulation of IL-1β and HBD-2.