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Infect Immun, March 1998, p. 932-937, Vol. 66, No. 3
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Regulation of Periodontal Ligament Cell Functions by Interleukin-1beta

Sudha Agarwal,1,* Charu S. Chandra,2 Nicholas P. Piesco,1 Herman H. Langkamp,1 Lathe Bowen,2 and Coskun Baran3

Division of Oral Biology1 and Division of Dental Surgical Sciences,2 University of Pittsburgh, Pittsburgh, Pennsylvania 15261, and Department of Periodontology, University of Gazi, Ankara, Turkey3

Received 13 May 1997/Returned for modification 7 July 1997/Accepted 16 December 1997

Periodontal ligament (PDL) cells maintain the attachment of the tooth to alveolar bone. These cells reside at a site in which they are challenged frequently by bacterial products and proinflammatory cytokines, such as interleukin-1beta (IL-1beta ), during infections. In our initial studies we observed that IL-1beta down-regulates the osteoblast-like characteristics of PDL cells in vitro. Therefore, we examined the functional significance of the loss of the PDL cell's osteoblast-like characteristics during inflammation. In this report we show that, during inflammation, IL-1beta can modulate the phenotypic characteristics of PDL cells to a more functionally significant lipopolysaccharide (LPS)-responsive phenotype. In a healthy periodontium PDL cells exhibit an osteoblast-like phenotype and are unresponsive to gram-negative bacterial LPS. Treatment of PDL cells with IL-1beta inhibits the expression of their osteoblast-like characteristics, as assessed by the failure to express transforming growth factor beta 1 (TGF-beta 1) and proteins associated with mineralization, such as alkaline phosphatase and osteocalcin. As a consequence of this IL-1beta -induced phenotypic change, PDL cells become responsive to LPS and synthesize proinflammatory cytokines. The IL-1beta -induced phenotypic changes in PDL cells were transient, as removal of IL-1beta from PDL cell cultures resulted in reacquisition of their osteoblast-like characteristics and lack of LPS responsiveness. The IL-1beta -induced phenotypic changes occurred at concentrations that are frequently observed in tissue exudates during periodontal inflammation (0.05 to 5 ng/ml). The results suggest that, during inflammation in vivo, IL-1beta may modulate PDL cell functions, allowing PDL cells to participate directly in the disease process by assuming LPS responsiveness at the expense of their normal structural properties and functions.


* Corresponding author. Mailing address: Division of Oral Biology, 579 Salk Hall, University of Pittsburgh, Pittsburgh, PA 15261-1964. Phone: (412) 648-8951. Fax: (412) 648-8219. E-mail: sagar+{at}pitt.edu.




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