Methods: CD1d-/- mice and C57BL/6J mice which were administered α-GC (α-Galactosylceramide) were orally infected with P. gingivalis strain W83 10 times at 3-day intervals. After 1day of the last infection, alveolar bone resorption, serum SAA level, serum P. gingivalis-specific antibody levels, and gene expressions in the liver were examined.
Results: Alveolar bone resorption was accelerated in the NKT cell-activated group (α-GC-administered mice). Meanwhile, the bone loss was not observed in the NKT cell-deficient group (CD1d-/- mice). Serum levels of SAA and P. gingivalis-specific antibodies were significantly higher in the NKT cell-activated group compared with the control group. In the liver, gene expressions of IFN-γ, IL-4, TNF-a, and RANKL were down-regulated in the NKT cell-deficient group, whereas up-regulated in the NKT cell-activated group.
Conclusion: NKT cells appear to play as effector cells, which result in the progression of alveolar bone resorption and systemic inflammatory responses in P. gingivalis infected mice.