The bacterial and/or host mechanisms involved in the near universal infection of the lungs of CF patients with P. aeruginosa have not been identified, d Previous studies from this and other labs showed that P. aeruginosa binding to cultured airway epithelial cells showed that the bacteria bound equally to CF and CFTR-corrected airway epithelia [17] and that binding occurred more prominently to the basolateral surfaces of epithelia with high transepithelial resistance and to regions near tight junctions in epithelia with low transepithelial resistance [18,19]. This evidence concerns the gene CFTR and cystic fibrosis.