Altogether, these data imply that AIM2 inflammasome-dependent IL-1α release is not correlated to the release of eicosanoids from PBMCs obtained from both exacerbated and stable COPD patients; rather, another novel mechanism, AIM2-dependent, may be responsible for the inflammatory pattern that leads to the exacerbation phase of COPD. Here, IL1A is linked to chronic obstructive pulmonary disease.