Methods: C57BL/6J (wild-type), CD1d-/-, and α-galactosylceramide (αGC)-simulated wild-type (NKT cell activated) mice were orally infected with P. gingivalis strain W83 10 times at 3-day intervals. After 1day of the last infection, we examined alveolar bone resorption; serum amyloid A (SAA), P. gingivalis-specific antibodies and RANKL levels in the sera; the levels of cytokine production by in vitro restimulation of splenocytes; and gene expressions in the liver were examined.
Results: Apart from the findings in CD1d-/- mice, the level of alveolar bone resorption was elevated by the infection and was further accelerated in the αGC-stimulated mice. Serum levels of SAA and P. gingivalis-specific antibodies were significantly higher in the αGC-stimulated mice compared with the wild-type mice. In the liver, the expression levels of the genes encoding IFN-γ, IL-4, TNF-α, and RANKL were down-regulated in the CD1d-/- mice, whereas the levels were up-regulated in the αGC-stimulated mice. Cytokine profile of splenocytes sifted from Th1 in wild-type to Th2 in αGC-stimulated mice.
Conclusion: NKT cells upregulate systemic and local inflammatory responses and participate in the progression of alveolar bone resorption in P. gingivalis-infected mice.