LPS Responsiveness in Periodontal Ligament Cells is Regulated by Tumor Necrosis Factor-α

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Abstract
Gingival fibroblasts function as accessory immune cells and are capable of synthesizing cytokines in response to lipopolysaccharides (LPS) from Gram-negative microbes. Recently, we have isolated, cloned, and characterized two cell lines which exhibit characteristics of periodontal ligament (PDL) cells. In this report, we demonstrate that PDL cells showing osteoblast-like phenotype are not LPSresponsive cells. However, treatment of PDL cells with tumor necrosis factor-α (TNF-a) inhibits the expression of their osteoblast-like characteristics. As a consequence of this TNF-a-induced phenotypic change, PDL cells become LPSresponsive, i.e., synthesize several pro-inflammatory cytokines in response to LPS. These phenotypic changes occur at concentrations of TNF-a that are frequently observed in tissue exudates during periodontal inflammation, suggesting a physiological significance for these in vitro observations. It is of interest that TNF-a-induced phenotypic changes in PDL cells are transient, since removal of rhTNF-a from the supernatants of PDL cell cultures results in re-acquisition of the osteoblast-like characteristics and lack of LPS responsiveness of PDL cells. These results suggest that TNF-a, by regulating the PDL cell functions, may allow these cells to participate in the disease process as accessory immune cells at the expense of their structural properties.