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1 Laboratorio di Genetica Molecolare and 3 Clinica Pediatrica, Istituto Giannina Gaslini, 16148 Genoa; 2 Istituto di Cibernetica e Biofisica, Consiglio Nazionale delle Ricerche, 16149 Genoa; and 4 Telethon Institute for Gene Therapy, Ospedale San Raffaele, 20132 Milan, Italy
Human bronchial epithelial cells were
treated in vitro with interferon-
or tumor necrosis factor-
to
assess their effect on transepithelial ion transport. Short-circuit
current measurements revealed that Na+ absorption was
markedly inhibited by interferon- (10-1,000 U/ml). The cystic
fibrosis transmembrane conductance regulator was also downregulated by
interferon- as evident at the protein level and by the decrease in
the cAMP-dependent current. On the other hand, interferon- caused an
increase of the current elicited by apical UTP application, which is
due to the activity of Ca2+-dependent Cl
channels. Tumor necrosis factor- caused few changes in ion
transport. Transepithelial fluid transport was measured in normal and
cystic fibrosis cells. At rest, both types of cells showed an
amiloride-sensitive fluid absorption that was inhibited by
interferon- but not by tumor necrosis factor-. Our results show
that interferon- alters the transepithelial ion transport of
cultured bronchial cells. This effect may change the ion composition
and/or volume of periciliary fluid.
airway surface fluid; sodium absorption; cystic fibrosis; airway epithelium; chloride transport
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