The effective repair of damage to the airway epithelium is essential to maintain the ability to exclude airborne particulates and protect against potential pathogens. Carbohydrates on the cell surface have an important role in cell-cell and cell substrate interactions. Using a model of repair with airway epithelial derived cells of the 16HBE 14o^- cell line, we have examined the effect of the Aleuria aurantia lectin (AAL) which binds very selectively to 1,6 linked fucose residues. Addition of unconjugated or FITC labelled AAL reduced the rate of epithelial repair to approximately one third of control values as measured by image analysis, while cell viability was maintained. Pulse labelling with FITC-AAL for 30 minutes followed by incubation in AAL-free medium caused similar inhibition of repair but could be reversed by addition of fucose up to 7 hours after AAL removal. By confocal microscopy, AAL binding was found to be on the apical but not basolateral surfaces of cells and internalisation of the labelled lectin was seen. Pre-incubation of the lectin with fucose prevented this effect. UEA I lectin, which is also fucose specific, resulted in similar binding to the cells and internalisation but did not effect the speed of the repair process. We conclude that 1,6 fucose binding sites play an important role in epithelial repair. Better understanding of this process will provide a deeper insight into the crucial mechanisms of epithelial repair.