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 M, Into T, Murakami Y. 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. Eur J Oral Sci 2010; 118: 574–581. © 2010 Eur J Oral Sci 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 .