In keeping with our previous studies [16]–[18], CXCL8 was chosen as it is generated upon activation of NF-κB and mitogen-activated protein kinase (MAPK)-dependent proinflammatory signaling, and as the principal mediator responsible for neutrophil recruitment is highly relevant to the pathology of asthma and COPD. Here, CXCL8 is linked to asthma.