Influence of Exogenous IL-12 on Human Periodontal Ligament Cells

Abstract

Periodontal disease is the most prevalent oral disease. The pathogenesis of this disease is mostly due to the robust host immune response, leading to the destruction of tooth-supporting tissue. Several cytokines have been shown to play roles in pathogenesis of periodontal disease; however, inflammatory cytokines can also activate the immunomodulatory properties of mesenchymal stem cells (MSCs), the mechanism to protect and maintain cell survival under inflammatory environment. Therefore, inflammation can exert both negative and positive effects for regulating tissue homeostasis. Interleukin 12 (IL-12) is one of the potent destructive stimulators in pathogenesis of many inflammatory diseases. In periodontitis, the increased level of IL-12 in serum and gingival crevicular fluid was found associated with the severity of the periodontal disease. However, the exact role of IL-12 in periodontitis is still unclear. The aim of this study was to investigate the responses of human periodontal ligament (PDL) cells to exogenous IL-12, especially on the immunomodulatory effects of IL-12. The results demonstrated the presence of IL-12 and IL-12 receptor (IL-12R) in periodontal tissues, and the expression was enhanced in tissues from periodontitis patients. Exogenous IL-12 stimulated the expression of some inflammatory cytokines as well as the immunomodulatory molecules, such as interferon gamma (IFNγ), human leukocyte antigen (HLA), and indoleamine-pyrrole-2,3-dioxygenase (IDO) enzyme. In conclusion, the data suggested the influence of increased IL-12, during periodontal inflammation, on controlling tissue’s homeostasis by upregulating the inflammatory cytokines and modulating the function of immune cells through the expression of immunosuppressive molecules.