Age-Related Inflammation Accelerates COPD Development

Premature aging of the lung cells plays a factor in pathogenesis.

Investigators are targeting the molecular causes of chronic obstructive pulmonary disease (COPD) in light of a lack of effective treatments that target the cause of the disease.

A study published recently in Oncotarget evaluated the underlying causes of COPD, specifically in the elderly population. The study noted that the inflammatory processes in lung tissue are a vital factor in the development of the disease.

"Our results show that age-related inflammatory changes play an important role in accelerated COPD development," said first author Gerrit John-Schuster, MD, in a press release.

It is believed COPD development is caused by a reaction in lung tissue from chronic exposure to toxic gases or particles, such as from cigarette smoke. The exposure results in excessive mucus production, cough, and remodeling processes in the airways. Toxic particles also cause the loss of alveoli, which is then subsequently not available for gas exchange.

The researchers also found that increased immune system activity plays a role in COPD development because the immune cell count in the lungs is significantly elevated. Premature aging in lung cells also supports the development of COPD, the study noted.

The researchers analyzed the influence of immune system cells on COPD development. In an animal model, an association was found between aging and increased inflammation processes, especially when the lung is also exposed to cigarette smoke.

"The current scientific consensus is that both aging and cigarette smoke facilitate the development of COPD. However, the mechanisms that lead to this remain unclear," study lead Ali Önder Yildirim said in a press release. "We have shown for the first time that the immune response, especially in the aged lung, plays an essential role in the pathogenesis of the disease. This provides us with new directions for the development of innovative approaches to treatment."