Severe gum disease has been identified as a factor contributing to the advancement of chronic obstructive pulmonary disease (COPD). Yet, the specifics of how this connection manifests within the immune system must be discovered. A recent publication in mSystems unveils a study elucidating the immune cells’ role in the microbial bridge between COPD and gum disease.
The investigation, conducted by a team at Sichuan University, China, highlighted how bacteria linked to gum disease could facilitate the progression of COPD by activating two crucial types of immune cells: γδ T cells and M2 macrophages. The focus on these mechanisms opens up potential avenues for preventing or managing COPD, according to researchers at the West China Hospital of Stomatology at Sichuan University.
Microbiologists Boyu Tang, PhD, and Yan Li, PhD, who spearheaded the study, suggest that enhancing periodontal treatment and explicitly targeting the inhibition of γδ T cells and M2 macrophages could offer a means to mitigate COPD’s progression.
Globally, COPD ranks as the sixth primary cause of death, as reported by the World Health Organization. While tobacco smoking is a predominant cause in wealthier nations, both smoking and household air pollution are significant contributors in countries with lower and middle incomes.
Periodontitis, a severe gum condition, stems from the accumulation of plaque, a bacterial film, which, if not addressed, can calcify into tartar, aggravating gum inflammation and leading to deep pockets between teeth and gums. This environment fosters bacterial growth and can result in bone loss. As a chronic infectious disease, periodontitis has been linked to various other health issues, including diabetes, hypertension, certain cancers, cardiovascular diseases, and COPD.
Li and Tang’s prior research established the significant role of the oral bacterium Porphyromonas gingivalis in gum disease. Their latest work utilized mouse models to demonstrate how this bacterium could exacerbate COPD progression. One part of their study showed that mice afflicted with both periodontitis and COPD experienced more severe COPD progression compared to those with COPD alone.
Further, the researchers discovered that in mice orally infected with P. gingivalis, the bacterium migrated to and infected the lungs, significantly altering the lung microbiota. Additional experiments revealed that periodontitis could expand immune cells in the lung tissue. Using mouse lung tissue in their experiments, the team established that P. gingivalis could trigger these immune cells, enhancing cytokine production linked to COPD aggravation.
Although the observed decline in lung function and rise in immune cell numbers were less than anticipated, this discrepancy might stem from the experimental conditions. The researchers created COPD models in mice through cigarette smoke exposure and suggested that extended exposure could amplify these effects. Li indicated plans for further research to explore how increased smoke exposure impacts the immune response.
The team is also preparing to validate their findings through studies involving human participants suffering from both conditions. They aim to assess the impact of periodontitis treatment on lung function and immune cell levels. This research could pave the way for a novel approach to treating COPD, offering hope for more effective management strategies.
More information: Kaixin Xiong et al, Periodontitis aggravates COPD through the activation of γδ T cell and M2 macrophage, mSystems. DOI: 10.1007/10.1128/msystems.00572-23
Journal information: mSystems Provided by American Society for Microbiology
