They also found that AIM2 inflammasome is at the crossroad between COPD and lung cancer in that its higher presence is correlated to lower survival rate of smoking COPD adenocarcinoma patients.

Dr. Rosalinda Sorrentino from The University of Salerno said, “Chronic Obstructive Pulmonary Disease (COPD) is characterized by chronic lung and systemic inflammation, associated with decline of lung function, airway remodeling and alveolar dysfunction.”

Almost 40% of COPD patients develop lung cancer, whereas cigarette smoke is at the basis of almost 90% of lung cancer establishment.

So researchers focused their attention on an inflammatory pathway, the inflammasome.

AIM2 inflammasome and caspase-11 underlie lung inflammation typical of smoking COPD patients who have a higher hazard ratio in terms of AIM2-related expression, implying lower survival rate than non-smoker, non-COPD adenocarcinoma patients.

The Sorrentino Research Team concluded in their Oncotarget Research Output, “we demonstrated that the exposure to first-hand smoking leads to emphysematous changes typical of human COPD and an inflammatory lung microenvironment which is associated to the non-canonical, caspase-11-dependent inflammasome pathway.

Although a direct correlation between AIM2 and caspase-11 was not proved in this manuscript, we found that according to the role of caspase-11, AIM2 inflammasome and IL-1£ are at the crossroad between COPD and lung cancer in that their expression are increased in our experimental model of COPD and human lung cancer samples.

Therefore, although some questions are still open on the role of AIM2 and caspase-11/IL-1£ in COPD, the data obtained so far pave the way for a novel scientific approach for COPD patients that develop lung cancer, focusing on the biology of the AIM2 inflammasome as a potential pharmacological target.”

Source: Medindia