# Periodontitis pathogen Porphyromonas gingivalis promotes chronic obstructive pulmonary disease via affecting neutrophils chemotaxis and function

## TL;DR

This study shows that the periodontitis bacterium Porphyromonas gingivalis worsens COPD by affecting neutrophil behavior and lung inflammation.

## Contribution

The study reveals a novel mechanism by which periodontitis pathogens contribute to COPD progression through neutrophil recruitment and activation.

## Key findings

- P. gingivalis translocates to the lungs and promotes neutrophil recruitment via chemokine secretion.
- Neutrophils activated by P. gingivalis release MMP-8 and NE, worsening lung inflammation and tissue damage.
- Periodontitis exacerbates COPD symptoms through bacterial-induced immune responses in the lungs.

## Abstract

Chronic obstructive pulmonary disease (COPD), a disease responsible for early mortality worldwide, is well accepted to be associated with periodontitis epidemiologically. Although both of the diseases are the multi-microbial inflammatory disease, the precise underlying mechanisms by which periodontitis influences the progression of COPD remains largely unknown. Here, we established COPD accompanied with periodontitis mouse models and observed the pronounced progress in pulmonary symptoms and histopathology, characterized by poorer respiratory function, thickened bronchial walls, and increased neutrophils infiltration in lung tissue. Mechanistically, periodontitis pathogen Porphyromonas gingivalis (P. gingivalis) relocated in the lung through the respiratory tract and LPS from P. gingivalis promoted the secretion of chemokines CXCL2 and G-CSF of alveolar epithelial cells through NF-κB and p38 MAPK pathways to recruit neutrophils. Furthermore, exposure to P. gingivalis of infiltrated neutrophils released matrix metallopeptidase-8 (MMP-8) and neutrophil elastase (NE), which aggravated airway inflammation and tissue damage. These findings indicated that periodontitis could exacerbate COPD via its pathogen P. gingivalis, which translocated in the lung and stimulated neutrophil chemotaxis and activation in the lung.