CFTR and cystic fibrosis: Several hypotheses can account for the exaggerated inflammatory responses of cells of CF patients: 1) that binding of bacterial LPS to cell surface CFTR normally elicits protective responses, e.g. phagocytosis and rapid initiation of signaling mediated by IL-1 [12], [23], 2) that alterations of glycosylation that are characteristic of the surfaces of CF cells sensitize them to P. aeruginosa, e.g. [6], or 3) that alteration of the composition of airway surface liquid by CFTR activity affects bacterial clearance.