Oral Pathogen Coaggregates With to Modulate the Inflammatory Cytotoxicity of Pulmonary Epithelial Cells.

Chronic obstructive pulmonary disease (COPD) is the third leading cause of mortality worldwide, and inflammatory damage induced by bacterial infections is an important contributor to the etiology of COPD. , a recognized periodontal pathogen, is considered as a biomarker of lung function deterioration of COPD patients coinfected with , but the underlying mechanism is still unclear. This study established single- and dual-species infection models, bacterial simultaneous and sequential infection models, and found that could coaggregate with to synergistically invade into pulmonary epithelial cells and transiently resist -induced cytotoxic damage to amplify IL-6 and TNF-α associated inflammation in pulmonary epithelial cells simultaneously infected with and . Furthermore, pretreatment or subsequential infection could maintain or even aggravate -induced inflammatory cytotoxicity of pulmonary epithelial cells. These results indicate that oral pathogen coaggregates with to facilitate bacterial invasion and modulates the inflammatory cytotoxicity of pulmonary epithelial cells, which may contribute to lung function deterioration of COPD patients accompanied with and coinfection.