Severe gum disease has been linked to the progression of chronic obstructive pulmonary disease, or COPD, but an understanding of how the connection plays out in the immune system remains unclear.
Now a new study by a team in China—and published in mSystems—identifies immune system cells that play a critical role in the microbial link between COPD and gum disease.
Researchers from Sichuan University report that bacteria associated with gum disease promote COPD through the activation of two types of cells, γδ T cells and M2 macrophages, that are important to the immune system.
“By enhancing periodontal therapy and targeting the inhibition of γδ T cells and M2 macrophages, [we] may be able to help control the progression of COPD,” study lead Dr Boyu Tang said.
Previous studies have established that the oral bacteria Porphyromonas gingivalis plays an important role in gum disease. For the new work, Professor Tang and colleagues 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.
The researchers noted that the decrease in lung function and increase in immune cells was more modest than they’d predicted, but that could be an artifact of the experimental set-up. The team created COPD animal models using exposure to cigarette smoke.
“If the cigarette smoke exposure could be extended for a longer period of time, these changes might be more pronounced,” Professor Li said.
In future studies, the group plans to investigate how increases in smoke exposure might affect the immune response.
“We’ll further carry out additional studies on human subjects to confirm the mechanism,” Professor Li said.
They plan to recruit patients with both conditions and offer periodontitis treatment, then compare lung function and immune cell counts before and after.
“Our finding could lead to a potential new strategy for treating COPD.”
