Open AccessExpression of NOD2 is increased in inflamed human dental pulps and lipoteichoic acid-stimulated odontoblast-like cells
Author(s) -
Jean-François Keller,
Florence Carrouel,
MarieJeanne Staquet,
Thomas A. Kufer,
C. Baudouin,
Philippe Msika,
Françoise Bleicher,
JeanChristophe Farges
Publication year - 2009
Publication title -
innate immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.921
H-Index - 69
eISSN - 1753-4267
pISSN - 1753-4259
DOI - 10.1177/1753425909348527
Subject(s) - lipoteichoic acid , nod2 , tlr2 , chemistry , odontoblast , inflammation , microbiology and biotechnology , immune system , biology , pulp (tooth) , tlr4 , immunology , bacteria , innate immune system , medicine , dentistry , staphylococcus aureus , genetics
Human odontoblasts trigger immune response s to oral bacteria that invade dental tissues during the caries process. To date, their ability to regulate the expression of the nucleotide-binding domain leucine-rich repeat containing receptor NOD2 when challenged by Gram-positive bacteria is unknown. In this study, we investigated NOD2 expression in healthy and inflamed human dental pulps challenged by bacteria, and in cultured odontoblast-like cells stimulated with lipoteichoic acid (LTA), a Toll-like receptor (TLR) 2 agonist which is specific for Gram-positive bacteria. We found that NOD2 gene expression was significantly up-regulated in pulps with acute inflammation compared to healthy ones. In vitro, LTA augmented NOD2 gene expression and protein level in odontoblast-like cells. The increase was more pronounced in odontoblast-like cells compared to dental pulp fibroblasts. Blocking experiments in odontoblast-like cells with anti-TLR2 antibody strongly reduced the NOD2 gene expression increase, whereas stimulation with the synthetic TLR2 ligand Pam 2 CSK 4 confirmed NOD2 gene up-regulation following TLR2 engagement. These data suggest that NOD2 up-regulation is part of the odontoblast immune response to Gram-positive bacteria and might be important in protecting human dental pulp from the deleterious effects of cariogenic pathogens.