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LPS Responsiveness in Periodontal Ligament Cells is Regulated by Tumor Necrosis Factor-
J.C. Quintero
Division of Oral Biology, 589 Salk Hall, University of Pittsburgh, Pittsburgh, PA 15261
N.P. Piesco
Division of Oral Biology, 589 Salk Hall, University of Pittsburgh, Pittsburgh, PA 15261
H.H. Langkamp
Division of Oral Biology, 589 Salk Hall, University of Pittsburgh, Pittsburgh, PA 15261
L. Bowen
Division of Dental Surgical Sciences, 589 Salk Hall, University of Pittsburgh, Pittsburgh, PA 15261
S. Agarwal
Division of Oral Biology, 589 Salk Hall, University of Pittsburgh, Pittsburgh, PA 15261
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- (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.
Key Words: periodontal ligament cells lipopolysaccharide tumor necrosis factor-
Journal of Dental Research, Vol. 74, No. 11,
1802-1811 (1995)
DOI: 10.1177/00220345950740111401

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