In support, in a mouse model of cigarette smoke-driven acute COPD, airway neutrophilia was dependent on the release of IL-1β/IL-18 - in a NLRP3/ASC and caspase 1/11-dependent manner; whereas IL-1α appeared to involve caspase 1/11 independently of IPAF, AIM2 and NLRP3 [56-61], implying other inflammasome-dependent and –independent mechanism/s. This evidence concerns the gene IL1A and chronic obstructive pulmonary disease.