Dr. Chiara Colarusso is currently a Post-Doctoral Researcher in Pharmacology at the Department of Pharmacy, University of Salerno. Her actual scientific interest is on the molecular/cellular mechanisms involved in chronic lung inflammation at the basis of lung diseases, such as COPD and lung cancer. In particular, she is being focusing on the inflammasome-dependent pathways puzzling from the process of lung cancer establishment up to progression that occurs after therapeutic treatment. In this regard, another goal she is trying to reach is to understand cellular and molecular mechanism/s at the basis of ICI’s resistance in lung cancer patients.
Abstract
Background. Epidemiological evidence indicate that almost 40% of COPD patients develop lung cancer; whereas cigarette smoke (CS), the leading cause and the most common risk factor for both COPD and lung cancer, is at the basis of almost 90% of lung cancer establishment. Aims and objectives. In our previous study we demonstrated AIM2 inflammasome drives the release of pro-inflammatory and pro-fibrotic factors involved in the exacerbation stage of COPD and that it could play a pro-carcinogenic role in lung cancer, in that its activation in tumor-associated plasmacytoid dendritic cells (pDCs) is associated to lung tumor cell proliferation. Methods. We took advantage of a mouse model of COPD induced by CS inhalation. We compared the murine data to human lung adenocarcinoma-derived samples stratified according to the smoking and COPD status. Results. We demonstrated that the exposure to first-hand smoking leads to emphysematous changes typical of human COPD, associated to bronchial tone impairment, collagen deposition and IL-1-like cytokine release. We found that AIM2 was involved in smoking-induced lung inflammation and COPD-like features in that its expression was higher in lung recruited DCs and macrophages of smoking mice compared to mice exposed to filtered air (control group). On the other hand, we found that AIM2 expression was higher in the cancerous tissues of lung cancer patients than non-cancerous (normal) tissues, independently of COPD and smoking status. Interestingly, higher expression of AIM2 in non-cancerous tissues of smoker lung cancer patients with COPD was associated to a higher hazard ratio of lower survival rate than patients who presented lower levels of AIM2. Conclusions. Our data imply that AIM2 inflammasome plays a role at the crosstalk between smoke-induced COPD and lung cancer, affecting patients’ survival.
COVID-19 and Respiratory System
Chronic Obstructive Pulmonary Disease and Asthma
Lung Cancer
Pneumonia
Cardio Pulmonary Disorders
Idiopathic Pulmonary Fibrosis
Interstitial Lung Disease
Lung Transplantation
Obstructive Sleep Apnea
Occupational Lung Diseases
Pulmonary Hypertension and Pulmonary Rehabilitation