Pretreatment of immortalized CF bronchial cells (NuLi) with IL-17 determined much greater IL-8 secretion in response to an agonist of NOD1, a cytosolic innate immune receptor, and P. aeruginosa diffusible material, identifying an amplification mechanism by which CF epithelial cells may trigger the inflammatory response to bacterial ligands [107]. This evidence concerns the gene CXCL8 and cystic fibrosis.