Suppressive effect of the antimicrobial peptide LL-37 on expression of IL-6, IL-8 and CXCL10 induced by Porphyromonas gingivalis cells and extracts in human gingival fibroblasts.
Inomata. Megumi M; Into. Takeshi T; Murakami. Yukitaka Y
Key Findings
- Live P. gingivalis doesn’t trigger inflammation in gingival fibroblasts, but killed bacteria do.
- LL‑37 suppresses the release of IL‑6 and IL‑8 from these cells when they’re exposed to bacterial components.
- LL‑37 also blocks activation of p38 and ERK pathways that lead to inflammatory gene expression.
Practical Outcomes
- LL‑37 or similar peptides might be useful in oral care products to reduce gum inflammation, but they’re not currently available as over‑the‑counter supplements. For now, the finding supports focusing on strategies that boost the body’s natural LL‑37 production (e.g., good oral hygiene, vitamin D) rather than direct dosing.
Summary
The body’s own antimicrobial peptide LL‑37 can calm down inflammation in gum cells caused by dead Porphyromonas gingivalis bacteria, lowering levels of IL‑6, IL‑8 and CXCL10 signals that drive gum disease.
Abstract
Porphyromonas gingivalis is a major periodontogenic bacterium and possesses immunostimulatory components, such as lipopolysaccharides (LPS) and fimbriae. The host antimicrobial peptide, LL-37, suppresses proinflammatory responses of immune cells but its effect on human gingival fibroblasts (HGFs) is not known. In this study, we assessed the effect of LL-37 on the proinflammatory responses of HGFs stimulated with P. gingivalis cells and their components. Live P. gingivalis cells did not induce proinflammatory responses of HGFs, and LL-37 did not alter these responses. However, LL-37 was able to suppress the killed P. gingivalis cell-induced secretion of interleukin (IL)-6 and IL-8. LL-37 also suppressed the expression of IL6, IL8, and CXCL10 genes that was induced by P. gingivalis components, including phenol-water extracts, lipid A, and fimbriae, and the induction of phosphorylation of p38 and extracellular signal-regulated kinase (ERK) by P. gingivalis lipopolysaccharide (LPS). CAMP was found to be expressed in oral epithelial cells but not in HGFs, despite stimulation with P. gingivalis components. Therefore, LL-37 can exert a suppressive effect on P. gingivalis-induced proinflammatory responses of HGFs in a paracrine manner, suggesting that excess inflammatory responses to P. gingivalis in the gingival tissue are suppressed by LL-37 in vivo.
Study Information
pubmed
2010
2010-09-30T00:00:00.000Z
10.1111/j.1600-0722.2010.00775.x
41
62