Proinflammatory nature of aspirated periodontopathic bacteria may cause pneumonia

Objectives: Aspiration pneumonia is a major health problem owing to its high mortality rate in elderly. The secretion of proinflammatory cytokines such as IL-8 and IL-6 by respiratory epithelial cells, which is induced by infection of respiratory bacteria such asStreptococcus pneumoniae, contributes to the onset of pneumonia. These cytokines thus play a key role in orchestrating inflammatory responses in the lower respiratory tract. Although emerging evidence has revealed an association between aspiration pneumonia and periodontitis, how periodontitis contributesto the onset of aspiration pneumonia remains unclear. Most periodontopathic bacteria are anaerobic and are therefore unlikely to survive in the lower respiratory organs of humans. Hence, we aimed to elucidate whether exposure to heat-inactivated periodontopathic bacteria induces proinflammatory cytokine production by several human respiratory epithelial cells, and in the lower respiratory organs and serum in mice.
Methods: Real-timePCRand ELISA were used to investigate in vitro induction by heat-inactivated periodontopathic bacteria and S. pneumoniaefor mRNA expression and protein production of proinflammatory cytokines by human respiratory epithelial cells.
ELISA was also used to determine in vivoinduction of cytokine production in the lower respiratory organs and serum of intratracheally heat-inactivated Fusobacterium nucleatum-inoculated mice.
Results: Some periodontopathic bacteria, especially F. nucleatum,strongly induced IL-8 and IL-6 production by BEAS-2Bbronchialepithelial cells. F. nucleatumalso induced IL-8 production by A549 alveolar epithelial cells as well as IL-8 and IL-6 production by Detroit 562 pharyngeal epithelial cells. Furthermore, F. nucleatum induced considerably higher cytokine production than S. pneumoniae. This was also observed in the entire lower respiratory organs and serum in mice.
Conclusions: F. nucleatumis a powerful inflammatory stimulant for respiratory epithelial cells and can stimulate cytokine production, thereby potentially contributingto the onset of aspiration pneumonia.