Study results show that the onset of chronic obstructive pulmonary disease (COPD) may be dictated by inflammatory processes in the lung tissue.
The onset of chronic obstructive pulmonary disease (COPD) may be dictated by inflammatory processes in the lung tissue, according to findings published in the journal Oncotarget.
Researchers from the German Research Center for Environmental Health examined mouse models exposed to cigarette smoke in order to prove their hypothesis that chronic cigarette smoke causes this lung tissue inflammatory process and, later, COPD. Characteristics of both young (two months) and old (12 months) mice were measured and the mice were exposed to cigarette smoke for three months.
The older mice which were exposed to the cigarette smoke developed increased lung compliance, emphysema, and airway remodeling compared to the mice not exposed to cigarette smoke. The young mice exposed to cigarette smoke did not display these qualities.
In the lung tissue analysis, the researchers discovered that there was a greater volume of inducible bronchus associated lymphoid tissue structures in the older mice after the cigarette exposure. The researchers extrapolated that age, in addition to cigarette exposure, was linked to the inflammatory process in the lung tissue and accelerated the onset and progression of COPD symptoms.
“The current scientific consensus is that both aging and cigarette smoke facilitate the development of COPD,” explained study leader Ali Önder Yildirim in a press release. “However, the mechanisms that lead to this remain unclear. 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.”
The statement continued by adding the lung tissue reacts to the cigarette smoke and toxin exposure by producing excessive mucus, coughing, and remodeling the airways. Additionally, the lungs lose alveoli, which are essential for gas exchange.
“Our results show that age related inflammatory changes play an important role in accelerated COPD development,” first author Gerrit John-Schuster concluded.