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Am J Physiol Lung Cell Mol Physiol 280: L482-L492, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 3, L482-L492, March 2001

Terminal sialylation is altered in airway cells with impaired CFTR-mediated chloride transport

Dianne Kube, Lynn Adams, Aura Perez, and Pamela B. Davis

Department of Pediatrics, Case Western Reserve University at Rainbow Babies and Children's Hospital, Cleveland, Ohio 44106

Reduced terminal sialylation at the surface of airway epithelial cells from patients with cystic fibrosis may predispose them to bacterial infection. To determine whether a lack of chloride transport or misprocessing of mutant cystic fibrosis transmembrane conductance regulator (CFTR) is critical for the alterations in glycosylation, we studied a normal human tracheal epithelial cell line (9/HTEo-) transfected with the regulatory (R) domain of CFTR, which blocks CFTR-mediated chloride transport; Delta F508 CFTR, which is misprocessed, wild-type CFTR; or empty vector. Reduced cAMP-stimulated chloride transport is seen in the R domain and Delta F508 transfectants. These two cell lines had consistent, significantly reduced binding of elderberry bark lectin, which recognizes terminal sialic acid in the alpha -2,6 configuration. Binding of other lectins, including Maakia amurensis lectin, which recognizes sialic acid in the alpha -2,3 configuration, was comparable in all cell lines. Because the cell surface change occurred in R domain-transfected cells, which continue to express wild-type CFTR, it cannot be related entirely to misprocessed or overexpressed CFTR. It is associated most closely with reduced CFTR activity.

cystic fibrosis; cystic fibrosis transmembrane conductance regulator; Delta F508; regulatory domain; lectins; fluorescent imaging; immunogold labeling; 3-(2,4-dinitroanilino)-3'-amino-N-methyldipropylamine


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