Therefore our hypothesis is that exacerbations of asthma and COPD during respiratory infections are due to ATP (a known danger associated molecular pattern) activating the P2X7/caspase-1 axis within EVs resulting in the release of IL-1β and IL-18, and subsequently increasing neutrophilia and worsening of symptoms that may accelerate disease pathogenesis. This evidence concerns the gene IL18 and respiratory tract infectious disorder.