Porphyromonas gingivalis induced inflammatory responses and promoted apoptosis in lung epithelial cells infected with H1N1 via the Bcl-2/Bax/Caspase-3 signaling pathway

The aim of the present study was to investigate the effects of Porphyromonas gingivalis (P. gingivalis) on inflammatory cytokine and nitic oxide (NO) production in lung epithelial cells infected with H1N1, and the underlying mechanisms. Lung epithelial cells were co-infected with P. gingivalis and H1N1. The concentrations of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 were detected via an ELISA, and the concentration of NO was detected by the nitrate reductive enzymatic method at 4, 8, 12 and 24 h following infection. The expression levels of inducible NO synthase (iNOS) was detected by western blotting. The apoptotic rate of lung epithelial cells was detected by flow cytometry. The relative protein expression levels of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax) and caspase-3 in lung epithelial cells were detected by western blotting. Compared with the control group, the concentration of the inflammatory cytokines TNF-α, IL-1β and IL-6 exhibited a significant increase (P<0.05) in the viral-infected, bacterial-infected and co-infected groups. The concentration of NO also increased significantly (P<0.05), along with the rise in the expression levels of iNOS (P<0.05) and the increase in the apoptosis rate of lung epithelial cells (P<0.05). The relative expression levels of caspase-3 and Bax proteins were increased significantly in the viral- and bacterial-infected groups when compared with the control. The relative expression levels of Bcl-2 protein exhibited a significant decrease in lung epithelial cells following the co-infection with P. gingivalis and H1N1 compared with the control (P<0.05). The results of the present study revealed that the combination of P. gingivalis and H1N1 infection in lung epithelial cells may promote the production of inflammatory cytokines and increase NO production, leading to increased levels of apoptosis in lung epithelial cells via the Bcl-2/Bax/caspase-3 signaling pathway.