Freeze fracture morphology of the tight junctions of the eccrine sweat gland from patients with cystic fibrosis.

The resorption of Na+ and Cl- across the duct of the human eccrine sweat gland is markedly decreased in individuals with cystic fibrosis (CF). Conceivably, a defective transcellular ion transport mechanism or an increased paracellular backflux of ions could account for the abnormal salt resorption in the sweat gland duct and other organs affected in CF. Tight junctions are thought to regulate paracellular ion flow. Specifically, the number of junctional elements observed by freeze fracture are believed to correspond with the extent of paracellular transport. We compared the freeze fracture morphology of tight junctions of eccrine sweat glands taken from 11 control and seven CF patients. In an attempt to "fingerprint" the junctions morphometrically, the following parameters were measured: the number of strands, the depth of the junction from the apical to the basal strand, the angle of intersection between strands, and the mean distance along a strand between intersections with two other strands. No significant difference was observed between control and CF sweat glands in the freeze fracture morphology of the tight junctions of the duct, the segment where the net reabsorption of Na+ and Cl- is abnormally decreased in CF. Significant changes were observed, however, in the means of the number of strands, the depth, and the distance between intersections for the tight junctions of the intercellular canaliculus of the secretory coil, which appears to function normally in CF.