krn-7000 and Bacteroidaceae-Infections

T and B cells are known to be involved in the disease process of periodontitis. However, the role of natural killer T cells in the pathogenesis of periodontitis has not been clarified.. To examine the role of these cells, C57BL/6J (wild-type), CD1d(-/-) and α-galactosylceramide (αGC)-stimulated wild-type mice were orally infected with Porphyromonas gingivalis strain W83.. Apart from CD1d(-/-) mice, the level of alveolar bone resorption was elevated by the infection and was further accelerated in αGC-stimulated mice. The infection induced elevated levels of serum amyloid A and P. gingivalis-specific IgG in the sera, although the degree of elevation was much smaller in the CD1d(-/-) mice. Infection-induced RANKL elevation was only observed in αGC-stimulated mice. Although the cytokines produced by splenocytes were mainly T-helper 1 type in wild-type mice, those in αGC-stimulated mice were predominantly T-helper 2 type. In the liver, the infection demonstrated no effect on the gene expression for interferon-γ, interleukin-4 and RANKL except αGC-stimulated mice in which the infection upregulated the gene expressions.. This study is the first to show that natural killer T cells upregulated systemic and local inflammatory responses induced by oral infection with P. gingivalis, thereby contributing to the progression of alveolar bone resorption.

Topics: Alveolar Bone Loss; Animals; Antibodies, Bacterial; Antigens, CD1d; Bacteroidaceae Infections; Galactosylceramides; Immunoglobulin G; Inflammation; Interferon-gamma; Interleukin-4; Killer Cells, Natural; Liver; Male; Mice, Inbred C57BL; Mice, Inbred Strains; Periodontitis; Porphyromonas gingivalis; RANK Ligand; Serum Amyloid A Protein; Spleen; Th1 Cells; Th2 Cells