Godfrey R W, Severs N J, Jeffery P K
Department of Lung Pathology, National Heart and Lung Institute, Royal Brompton Hospital, London, United Kingdom.
Am J Respir Cell Mol Biol. 1993 Aug;9(2):148-56. doi: 10.1165/ajrcmb/9.2.148.
Previous descriptive freeze-fracture studies have suggested that the airway epithelium in cystic fibrosis (CF) is associated with proliferation and basal extension of tight junctional elements. The significance of these reports in CF has been difficult to evaluate because tight junctions are labile structures, capable of alteration, postmortem. The aim of the present study was to test the hypothesis that the abnormalities in tight junction structure reported previously are unique to CF airways, and to determine the confounding effects of postmortem autolysis. To this end, we analyzed human airway epithelial tight junctions in: (1) histologically normal tissue taken from lungs resected for pulmonary tumor (i.e., resection controls), (2) lungs from patients who died of nonrespiratory causes (i.e., postmortem controls), (3) lungs removed from CF patients undergoing transplantation, and (4) lungs from CF patients postmortem. Tight-junctional depth, strand number, and junctional complexity were analyzed. Basal extensions and isolated foci of tight-junctional elements were found in all groups except for the resection controls. The following two parameters were therefore assessed: (1) the number of times a junction extended below the maximal depth found in the resection controls and (2) the extent of junctional elements that were isolated and distant from the apico-lateral junctional belt. The mean frequencies of occurrence of junctional extension beyond the normal maximum were 4.8% for the CF transplant, 23.6% for the control postmortem, and 48.8% for the CF postmortem group.(ABSTRACT TRUNCATED AT 250 WORDS)