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Infect Immun, March 1998, p. 932-937, Vol. 66, No. 3
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-1
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Copyright © 1998, American Society for Microbiology. All rights reserved.
Regulation of Periodontal Ligament Cell Functions by
Interleukin-1
(IL-1
), during infections. In
our initial studies we observed that IL-1
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-1
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-1
inhibits the expression of their osteoblast-like characteristics, as assessed by the failure to express transforming growth factor
1 (TGF-
1) and proteins associated with
mineralization, such as alkaline phosphatase and osteocalcin. As a
consequence of this IL-1
-induced phenotypic change, PDL cells become
responsive to LPS and synthesize proinflammatory cytokines. The
IL-1
-induced phenotypic changes in PDL cells were transient, as
removal of IL-1
from PDL cell cultures resulted in reacquisition of
their osteoblast-like characteristics and lack of LPS responsiveness. The IL-1
-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-1
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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