[P1-2-49] Brain dysfunction induced by Porphyromonas gingivalis and neutrophils in a mouse periodontitis model
Keywords:歯周病原細菌、好中球、脳機能障害
Purpose Porphyromonas gingivalis, the periodontopathic bacteria, is closely involved in the pathogenesis of chronic periodontitis. On the other hand, neutrophils in the oral cavity play an essential role in the defense against infection. However, P. gingivalis and neutrophils have also been implicated in the pathogenesis of brain dysfunction. The present study used periodontitis mouse models to examine the effects of P. gingivalis infection and neutrophil activation on brain function.
Materials and Methods The mouse model of periodontitis was based on C57BL/6 mice ligated with silk strings on the molars and then orally infected with P. gingivalis. The spread of P. gingivalis infection to the brain, proinflammatory cytokine expression, and citrullinated histone H3 (cit-H3) expression in the gingiva and brain were analyzed by RT-qPCR. The effects of periodontitis on brain function were assessed by a novel object recognition test.
Results P. gingivalis orally infection induced alveolar bone resorption and increased expression of proinflammatory cytokines and cit-H3 in the LIP mice. P. gingivalis spread to the brain, induced inflammatory responses, and impaired cognitive function in the LIP mice. These effects were abolished in the LIP mice infected with P. gingivalis gingipain-deficient strain or pretreated with DNase, suggesting that gingipains and neutrophils in the oral cavity may be involved in brain dysfunction.
Conclusion In periodontitis, P. gingivalis infection leads to the activation of oral neutrophils, which induces inflammation and dysfunction of the brain.
Materials and Methods The mouse model of periodontitis was based on C57BL/6 mice ligated with silk strings on the molars and then orally infected with P. gingivalis. The spread of P. gingivalis infection to the brain, proinflammatory cytokine expression, and citrullinated histone H3 (cit-H3) expression in the gingiva and brain were analyzed by RT-qPCR. The effects of periodontitis on brain function were assessed by a novel object recognition test.
Results P. gingivalis orally infection induced alveolar bone resorption and increased expression of proinflammatory cytokines and cit-H3 in the LIP mice. P. gingivalis spread to the brain, induced inflammatory responses, and impaired cognitive function in the LIP mice. These effects were abolished in the LIP mice infected with P. gingivalis gingipain-deficient strain or pretreated with DNase, suggesting that gingipains and neutrophils in the oral cavity may be involved in brain dysfunction.
Conclusion In periodontitis, P. gingivalis infection leads to the activation of oral neutrophils, which induces inflammation and dysfunction of the brain.