Gum disease worsens chronic obstructive pulmonary disease

Washington, DC — Severe gum disease has been linked to the development of chronic obstructive pulmonary disease, or COPD, but understanding how the connection plays out in the immune system remains unclear. This week on mSystems, a new study identifies immune system cells that play a critical role in the microbial link between COPD and gum disease.

Researchers from Sichuan University, China, report that bacteria associated with gum disease promote COPD by activating 2 types of cells, γδ T cells and M2 macrophages, that are important for the immune system. Focusing on this mechanism may provide new, practical strategies to prevent or control COPD, said the researchers, from the West China Hospital of Dentistry at Sichuan University.

“By enhancing periodontal therapy and targeting inhibition of γδ T cells and M2 macrophages [we] may help control the progression of COPD,” said microbiologist Boyu Tang, Ph.D., who led the study with microbiologist Yan Li, Ph.D.

According to the World Health Organization, COPD is the sixth leading cause of death worldwide. It is not curable. In higher income countries, smoking is the leading cause of COPD. In low- and middle-income countries, both smoking and household air pollution are important risk factors.

Periodontitis is a gum disease that results from the build-up of untreated plaque, a sticky film made up mostly of bacteria. Over time, plaque can harden into tartar and cause irritation and inflammation of the gum tissue, then create deep gaps between the teeth and gums where bacteria thrive and can lead to bone loss. Periodontitis is a chronic infectious disease, and previous studies have found it to be a risk factor for a number of diseases, including diabetes, hypertension, certain cancers, cardiovascular disease, and COPD.

Previous studies, including some led by Li and Tang, have demonstrated that the oral bacterium Porphyromonas gingivalis plays an important role in gum disease. For the new work, Li, Tang and colleagues used mouse models to show how these bacteria could worsen the progression of COPD. In one experiment, they showed that mice infected with both periodontitis and COPD had worse progression of COPD than mice infected only with COPD.

In another experiment, they found that in mice orally infected with P. gingivalis, the bacteria migrated and infected the 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 immune cells in lung tissue. Finally, in experiments using mouse lung tissue, the team connected the dots by showing that P. gingivalis could activate immune system cells, promoting their ability to produce cytokines associated with worsening COPD.

The researchers observed that the decrease in lung function and increase in immune cells was more modest than they had predicted, but this could be an artifact of the experimental setup. The team created animal models of COPD using exposure to cigarette smoke. “If exposure to cigarette smoke could be extended for a longer period of time, these changes may be more pronounced,” Lee said. In future studies, Li said the team plans to investigate how increasing exposure to smoke might affect the immune response.

“We will further conduct additional human studies to confirm the mechanism,” 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 the treatment of COPD.”