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Treponema denticola lipooligosaccharide activates gingival fibroblasts and upregulates inflammatory mediator production
Author(s) -
Tanabe Shinichi,
Bodet Charles,
Grenier Daniel
Publication year - 2008
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21447
Subject(s) - treponema denticola , porphyromonas gingivalis , matrix metalloproteinase , connective tissue , periodontitis , inflammation , fibroblast , prostaglandin e2 , immune system , chemistry , immunology , microbiology and biotechnology , biology , medicine , pathology , biochemistry , in vitro
In response to bacterial challenges, fibroblasts, a major constituent of gingival connective tissue, can produce immunoregulatory cytokines and proteolytic enzymes that may contribute to tissue destruction and the progression of periodontitis, a chronic inflammatory disease affecting tooth‐supporting tissues, including alveolar bone. The spirochete Treponema denticola is a major etiological agent of periodontitis and can invade oral tissues. The aim of the present study was to investigate the inflammatory response of gingival fibroblasts to T. denticola lipooligosaccharide (LOS). T. denticola LOS induced significant production of various inflammatory mediators by fibroblasts, including interleukin‐6, interleukin‐8, monocyte chemoattractant protein 1, nitric oxide, and prostaglandin E 2 . In addition, the secretion of matrix metalloproteinase 3, an enzyme active on basement membrane components, was also significantly increased. The response of fibroblasts was dose‐dependent and much stronger following a 24 h stimulation period. The expression and/or phosphorylation state of several signaling proteins, including Fos, MKK1, MKK2, MKK3/6, NF‐κB p50, and NF‐κB p65, was enhanced following stimulation of fibroblasts with T. denticola LOS. In summary, T. denticola LOS induced an inflammatory response in gingival fibroblasts and may thus contribute to the immunopathogenesis of periodontitis and the progression of the disease. J. Cell. Physiol. 216: 727–731, 2008, © 2008 Wiley‐Liss, Inc.