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Updated: May 5, 2026
A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
Porphyromonas gingivalis inducing autophagy-related biological dysfunction in alveolar epithelial cells: an in vitro
Qian Zhao1, Xueyuan Wang1, Wenyan Liu2
1Department of Stomatology, Beijing Chao-Yang Hospital, Capital Medical University, 8 Gongti South Road, Chaoyang District, Beijing, 100020, China.
Background:
Chronic obstructive pulmonary disease (COPD) is a respiratory disease with high morbidity and mortality. Notably, the pathogenesis and progression of COPD are related to lung infection, inflammatory response, and biological dysfunction in alveolar epithelial cells. Studies also found that periodontitis is an independent risk factor for COPD. The inhalation of periodontal pathogens into the respiratory system is the most common method for periodontal pathogens to promote the development of COPD. Porphyromonas gingivalis (P. gingivalis), the keystone pathogen in periodontitis, has been found to migrate to the lungs, triggering inflammatory reactions and causing decreased lung function. However, the impact of P. gingivalis infection on the biological function of alveolar epithelial cells remains unclear. Therefore, this study aimed to investigate the effects of P. gingivalis infection on the biological functions of alveolar epithelial cells.
Methods:
Mouse alveolar epithelial cells (MLE-12) were co-cultured with P. gingivalis and treated with autophagy inhibitor chloroquine (CQ) or LC3 siRNA in vitro. MTT assay and EdU staining were used to detect cell viability, and the TUNEL assay kit and Annexin V-FITC/PI method were used to detect cell apoptosis. Western blot was used to detect autophagic markers LC3 and P62, and mRFP-GFP-LC3 was used to observe autophagic flux.
Results:
P. gingivalis inhibited the viability of alveolar epithelial cells in a dose- and time-dependent manner. P. gingivalis also promoted autophagy and apoptosis of alveolar epithelial cells in a dose-dependent manner. Interestingly, we found that inhibiting autophagy using CQ or silencing LC3 with siRNA significantly reduced cell apoptosis and viability damage induced by P. gingivalis. Thus, these data indicated the synergistic effect of autophagy in P. gingivalis-induced biological dysfunction of alveolar epithelial cells.
Conclusion:
P. gingivalis infection can cause biological dysfunction of alveolar epithelial cells, manifested as decreased cell viability, increased autophagy and apoptosis. Notably, the up-regulation of autophagy induced by P. gingivalis plays a synergistic role in this dysfunction.
