PT - JOURNAL ARTICLE AU - Chiara Colarusso AU - Michela Terlizzi AU - Aldo Pinto AU - Rosalinda Sorrentino TI - The inhibition of caspase-11 could prevent lung cancer in smoking mice AID - 10.1183/13993003.congress-2021.PA1120 DP - 2021 Sep 05 TA - European Respiratory Journal PG - PA1120 VI - 58 IP - suppl 65 4099 - http://erj.ersjournals.com/content/58/suppl_65/PA1120.short 4100 - http://erj.ersjournals.com/content/58/suppl_65/PA1120.full SO - Eur Respir J2021 Sep 05; 58 AB - Background: Cigarette smoke (CS) is the main risk factor for the development of both chronic obstructive pulmonary disease (COPD) and lung cancer (Colarusso, C. et al Oncotarget 2017; 8(47):81813-818241).Aims and objectives: In our preliminary study we proved that caspase-11 is involved in lung cancer progression (Terlizzi, M. et al. J Exp Clin Cancer Res 2020; 39(1):2422). Therefore, the aim of this study was to understand whether smoking exposure could involve the activation of caspase-11, responsible of lung cancer establishment.Methods: To pursue the goal of this study, we exposed C57Bl/6N and 129Sv mice for 4-8-16 weeks to first-hand smoking in order to mimic the inhalation profile of human smokers.Results: CS exposure led to alveolar enlargement, deposition of collagen and mucus production, and the release of IL-1-like cytokines in C57Bl/6N mice. The genetic alteration of caspase-11 in 129Sv mice significantly reduced collagen deposition as well as the release of IL-1-like cytokines, highly associated to tumor progression. These data were correlated to smoking NSCLC patients who had a worse survival rate according to the positivity to caspase-4, the human analogue of the murine caspase-11.Conclusions: Our data demonstrate that caspase-11 is at the crossroad between smoking-induced lung latent inflammation and lung cancer establishment.FootnotesCite this article as: European Respiratory Journal 2021; 58: Suppl. 65, PA1120.This abstract was presented at the 2021 ERS International Congress, in session “Prediction of exacerbations in patients with COPD”.This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).