Elucidation of autoummune condition in periodontitis-accelerated atherosclerosis and control by oral tolerance

不仅活细菌参与了牙周病细菌对动脉粥样硬化的加速作用，而且参与了细胞成分如脂多糖的作用，并影响TLR、MLR和氧化应激(HSP)的表达。牙周感染引起的自身抗原的增加与临床标本中自身抗体的增加呈TLR依赖性，提示牙周病原菌对低密度脂蛋白的氧化修饰导致自身免疫紊乱。相反，牙周感染GroEL通过减少炎症标志物和自身免疫标志物来抑制动脉粥样硬化。这些结果表明，口服耐受诱导对减轻动脉硬化是有效的。

Not only live bacteria but also the cellular components, such as LPS have been participated in acceleration of the atherosclerosis by periodontopathic bacteria,and affected expression of TLR,MLR and oxidant stress,or HSP. The increase in autoantigens by periodontal infection was TLR dependent and correlated with the increase in autoantibody in clinical samples.Furthermore, it was suggested that oxidative modefication of LDL by periodontopathic bacteria induced autoimmune disorder.In contrast, immunization with P.gingivalis GroEL suppressed atherosclerosis with the reduction of inflammatory markers and autoimmune markers. These results suggest that oral tolerance induction is effective in reducing arteriosclerosis.