Increased oxidative stress in the cystic fibrosis airway. Constitutive NF-κB–mediated production of chemokines, including IL-8, leads to PMN recruitment, which persist in the airway, increasing the oxidative burden in the lung. Oxidative stress activates MAPK signaling pathways in the cystic fibrosis epithelium, amplifying the production of IL-8 and, therefore, recruiting additional PMNs. Mutant CFTR in the epithelial cells is unable to channel the antioxidants GSH and SCN− into the airway, limiting its ability to counteract the oxidative stress. Because SCN− also has antimicrobial properties, bacterial killing in the airway is diminished as well.