Caspase-11 and AIM2 inflammasome involved in COPD and lung adenocarcinoma

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Oncotarget

published “Caspase-11 and AIM2 inflammasome are involved in smoking-induced COPD and lung adenocarcinoma” which reported that cigarette smoking is the leading risk factor for COPD and lung cancer establishment.

Epidemiologically, COPD patients are 6.35 times more likely to develop lung cancer.

To mimic COPD, the authors exposed mice to nose-only cigarette smoke and used human samples of lung adenocarcinoma patients according to the smoking and COPD status.

Interestingly, higher expression of AIM2 in non-cancerous tissue of smoking COPD adenocarcinoma patients was correlated to a higher hazard ratio of poor survival rate than in patients who presented lower levels of AIM2.

The Oncotarget authors 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.

The Oncotarget authors 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 remodelling and alveolar dysfunction.”

Inhalation of cigarette smoke is the main risk factor for the development of COPD, but it is also the main risk factor for the development of lung cancer.

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

Therefore, in the attempt to understand the crosstalk between smoking, COPD and lung cancer, which have been demonstrated as associated with inflammation, they focused our attention on an inflammatory pathway, the inflammasome.

Therefore, in the attempt to understand the role of the AIM2 inflammasome in smoking-induced COPD and COPD-induced lung cancer, they took advantage of a cigarette smoking model that could mimic COPD in mice, as already demonstrated by Beckett et al.,.

The authors found that 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 (caspase-4 in humans) [11, 16, 17, 27], AIM2 inflammasome and IL-1α 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 [11]. Therefore, although some questions are still open on the role of AIM2 and caspase-11/IL-1α 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.”

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