Porphyromonas gingivalis (Pg) is a highly pathogenic causative bacteria of periodontal disease and causes aspiration pneumonia. COPD patients often have aspiration pneumonia and Pg was detected from patients? tracheal aspirates. However, the effect of Pg on respiratory system and COPD pathology is unknown. Here, we aimed to elucidate the molecular mechanism of aspiration pneumonia caused by Pg and examined the effect of Pg on normal or COPD model cells and mice.
We used ?/?ENaC-16HBE14o- cells and C57BL/6J-?ENaC-Tg mice as COPD model cells and mice, respectively. Epithelial Na+ channel (ENaC) is overexpressed in these models, and the expression of ENaC corelated to COPD severity. To mimic infection of Pg we used culture supernatant of Pg (PCS) that included many pathogenic factors. We found enhanced ENaC activity in PCS-treated COPD model cells. We also found increased inflammatory cytokines in normal human airway epithelial cells (16HBE14o-) and COPD model cells treated with PCS. Interestingly, inflammation was more remarkable in COPD model cells. Moreover, we found that protease-activated receptor-2 is involved in this inflammation and ENaC activation. We intratracheally administered PCS for 30 days to WT and COPD model mice and observed accumulation of immune cells especially macrophages in the lung tissues in both PCS-treated groups. Respiratory function was decreased mostly in PCS-treated COPD model mice.
This study provides experimental and scientific support that Pg infection in COPD lungs can cause acute exacerbations due to aspiration. These results raise the importance of research focusing on the "periodontal disease-COPD linkage" which is a serious health concern in aging society.