Vitamin D reduces the inflammatory response by Porphyromonas gingivalis infection by modulating human beta-defensin-3 in human gingival epithelium and periodontal ligament cells.

Periodontitis is a multifactorial polymicrobial infection characterized by a destructive inflammatory process. Porphyromonas gingivalis, a Gram-negative black-pigmented anaerobe, is a major pathogen in the initiation and progression of periodontitis; it produces several virulence factors that stimulate human gingival epithelium (HGE) cells and human periodontal ligament (HPL) cells to produce various inflammatory mediators. A variety of substances, such as vitamin D, have growth-inhibitory effects on some bacterial pathogens and have shown chemo-preventive and anti-inflammatory activity. We used a model with HGE and HPL cells infected with P. gingivalis to determine the influence of vitamin D on P. gingivalis growth and adhesion and the immunomodulatory effect on TNF-alpha, IL-8, IL-12 and human-beta-defensin 3 production. Our results demonstrated, firstly, the lack of any cytotoxic effect on the HGE and HPL cells when treated with vitamin D; in addition, vitamin D inhibited P. gingivalis adhesion and infectivity in HGE and HPL cells. Our study then showed that vitamin D reduced TNF-alpha, IL-8, IL-12 production in P. gingivalis-infected HGE and HPL cells. In contrast, a significant upregulation of the human-beta-defensin 3 expression in HGE and HPL cells induced by P. gingivalis was demonstrated. Our results indicate that vitamin D specifically enhances the production of the human-beta-defensin 3 antimicrobial peptide and exerts an inhibitory effect on the pro-inflammatory cytokines, thus suggesting that vitamin D may offer possible therapeutic applications for periodontitis.