IL-22 enhances CCL20 production in IL-1β-stimulated human gingival fibroblasts.

CC chemokine ligand 20 (CCL20) is involved in the recruitment of Th17 cells and thus in the exacerbation of periodontal disease, but the effect of simultaneous interleukin (IL)-22 and IL-1β stimulation on CCL20 production in human gingival fibroblasts (HGFs) is uncertain. In this study, we investigated the mechanisms of IL-1β- and/or IL-22-induced CCL20 production in HGFs. A single stimulation of IL-22 could not induce CCL20 production. On the other hand, IL-22 could increase CCL20 production from IL-1β-stimulated HGFs in a dose-dependent manner. C-Jun N terminal kinase (JNK) and inhibitor of nuclear factor κB (IκB)-α phosphorylation were increased in IL-1β- and IL-22-stimulated HGFs. An inhibitor of nuclear factor (NF)-κB decreased IL-1β- and IL-22-induced CCL20 production, though an inhibitor of JNK did not modulate CCL20 production. These data suggest that IL-1β in cooperation with IL-22 could increase Th17 cell accumulation in periodontally diseased tissues to enhance CCL20 production in HGFs.