Effects of TNF-a, IFN-c and IL-b on normal human bronchial epithelial cells. C. Kampf, A.J. Relova, S. Sandler, G.M. Roomans. #ERS Journals 1999. ABSTRACT: Several diseases affecting the airways such as asthma are associated with both epithelial damage and increased levels of pro-inflammatory cytokines. To investigate the possible relation between cytokines and epithelial damage, the effects of tumour necrosis factor-a (TNF)-a, interferon gamma (IFN-c) and interleukin-1 beta (IL-1b) on normal human bronchial epithelial cells in vitro were studied.The cells were exposed to these cytokines for 48 or 72 h, followed by morphological, immunohistochemical and metabolic studies.Transmission and scanning electron microscopical analyses demonstrated damage to the mitochondria and an increase in cell processes induced by the cytokines. The use of antibodies against desmosomal cytokeratin showed a decrease in desmosome formation in IFN-c-exposed cells. Decreased glucose oxidation rate and increased accumulation of nitric oxide were found in cytokine-exposed cells. N v -monomethyl-Larginine (L-NMMA) reduced nitrite production. X-ray microanalysis showed an increase in the intracellular sodium/potassium ratio of the cells after exposure to cytokines, which is an indication of cell damage. The cytokines induced both necrosis and apoptosis to varying degrees. IFN-c and TNF-a generally potentiate each other's effects.In conclusion tumour necrosis factor-a and interferon gamma, and to a lesser extent interleukin-1b, can cause damage to epithelial cells, which may be a factor involved in epithelial shedding in airway diseases.
Proliferation and death of airway epithelial cells may be of importance in the pathogenesis of asthma. T-helper (Th)-2 response interleukins (IL)-4, -5, and -13 have the ability to induce proliferation of airway epithelial cells.
Effect of luminal osmolarity on ion content of connective tissue in rat trachea after epithelial damage. A.J. Relova, G.M. Roomans. #ERS Journals Ltd 2001. ABSTRACT: The authors investigated the physical role of the airway epithelium in response to changes in the airway surface fluid9s composition by superperfusing the lumen with nonisotonic solutions. Morphological studies and measurements of changes in ion content in the underlying connective tissue (CT) were carried out.The study used an experimental model of isolated rat trachea. The trachea was mounted in an extraluminal organ bath with Ringer9s solution, whereas the lumen was perfused with a fluid in which the NaCl concentration was varied. The tissue was fixed for electron microscopy or frozen for X-ray microanalysis.X-ray microanalysis showed that the Na and Cl content of the CT increased with increasing luminal NaCl concentrations. This increase was significantly larger when the tight junctions had been damaged by exposure to ethylene glycol tetra-acetic acid. At high luminal NaCl concentrations, electron microscopy showed that a significant influx of fluid into the CT had occurred in tracheae with damaged epithelia. Damage to the epithelium also resulted in ultrastructural changes in myofibroblasts, increased diameter of capillaries, and thickening of the basement membrane.The epithelium evidently plays a crucial role in the regulation of the ion content of the connective tissue in the airway wall, and epithelial damage may explain the greater sensitivity to provocation with hypersomolar sodium chloride solutions or airway dehydration observed in patients with asthma or cystic fibrosis.
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