Porphyromonas gingivalis-induced autophagy exacerbates abnormal lung homeostasis: An in vivo and in vitro study

The aim of this study was to evaluate the effect of periodontal Porphyromonas gingivalis (P. gingivalis) infection on lung homeostasis and to explore the underlying mechanism.

In in vivo experiments, twelve mice were divided into two groups. The P. gingivalis infection group received P. gingivalis around the maxillary second molar, and the control group was left untreated. After 12 weeks, the histopathological changes of the lung tissue and the autophagy and apoptosis in the lung tissue cells were detected. In in vitro experiments, alveolar epithelial cell A549 was co cultured with P. gingivalis and treated with autophagy inhibitor chloroquine (CQ). Western blot was then used to detect autophagic markers LC3 and P62, and mRFP-GFP-LC3 was used to observe autophagic flux. Cell viability and apoptosis were also detected.

For the in vivo experiments, pathological changes were observed in the lung tissue of the P. gingivalis infection group at 12 weeks, along with higher levels of autophagy and apoptosis in the lung tissue cells. For the in vitro experiments, infection of alveolar epithelial cells with P. gingivalis inhibited cell viability and promoted cell autophagy and apoptosis. Interestingly, we found that inhibiting P. gingivalis-activated autophagy significantly improved cell apoptosis and viability damage induced by P. gingivalis.

Periodontal P. gingivalis infection can cause pathological changes and abnormal homeostasis in lung tissue, and the up-regulation of autophagy induced by P. gingivalis may play a synergistic role in this process.