How poor oral health can worsen fatal lung disease
While there is a connection between periodontitis and the progression of COPD, the precise impact on the immune system remains unclear.
Beijing: Researchers have identified immune system cells that play a critical role in how periodontitis — a severe gum disease worsens chronic obstructive pulmonary disease (COPD) — a potentially fatal lung disease.
Periodontitis has been linked to the progression of COPD but an understanding of how the connection plays out in the immune system remains unclear.
Researchers from Sichuan University in China report that bacteria associated with gum disease promote COPD through the activation of 2 types of cells, Gamma delta T cells and M2 macrophages, that are important to the immune system.
Focusing on this mechanism might offer new, practical strategies for COPD prevention or control, they said in the paper published in the journal mSystems.
“By enhancing periodontal therapy and targeting the inhibition of Gamma delta T cells and M2 macrophages [we] may be able to help control the progression of COPD,” said microbiologist Boyu Tang, doctoral student at West China Hospital of Stomatology at Sichuan University.
According to the World Health Organization, COPD is the sixth-leading cause of death worldwide. It is not curable. In higher-income countries, tobacco smoking is the leading cause of COPD; in low- and middle-income countries, both tobacco smoking and household air pollution are significant risk factors.
Periodontitis is a gum disease that results from the untreated buildup of plaque, a sticky film made primarily of bacteria. Over time, the plaque can harden into tartar and cause irritation and inflammation of gum tissue, and then produce deep gaps between the teeth and gums where bacteria flourish and may lead to bone loss.
For the study, the team used mouse models to show how those bacteria could aggravate progression of COPD. In one experiment, they showed that mice infected with both periodontitis and COPD had worse progression of COPD than mice infected with COPD alone.
In another experiment, they found that in mice orally infected with P. gingivalis, the bacteria migrated to and infected lung tissue, leading to a significant, observable change in the lung microbiota.
Further observations using flow cytometry and immunofluorescence revealed that periodontitis promoted the expansion of the immune cells in the lung tissue. Finally, in experiments using mouse lung tissue, the group connected the dots by showing that P. gingivalis could activate the immune cells, promoting their ability to produce cytokines associated with worsening COPD.
In future studies, the team plans to investigate how increases in smoke exposure might affect the immune response.
