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Laboratorio di Genetica Molecolare, Istituto Giannina Gaslini, Genova, Italy;
Institut National de la Santé et la Recherche Médicale, Unité 468, Service de Biochimie et Génétique, Hôpital Henri Mondor, Créteil, France; and
Laboratorio di Patologia Molecolare, Centro Regionale Fibrosi Cistica, Verona, Italy
Recent data show that proinflammatory stimuli may modify
significantly ion transport in the airway epithelium and therefore the
properties of the airway surface fluid. We have studied the effect of
IL-4, a cytokine involved in the pathogenesis of asthma, on
transepithelial ion transport in the human bronchial epithelium in
vitro. Incubation of polarized bronchial epithelial cells with IL-4 for
6–48 h causes a marked inhibition of the amiloride-sensitive
Na+ channel as measured in short circuit current
experiments. On the other hand, IL-4 evokes a 2-fold increase in the
current activated by a cAMP analog, which reflects the activity of the
cystic fibrosis transmembrane conductance regulator (CFTR). Similarly,
IL-4 enhances the response to apical UTP, an agonist that activates
Ca2+-dependent Cl- channels. These effects are
mimicked by IL-13 and blocked by an antagonist of IL-4R
. RT-PCR
experiments show that IL-4 elicits a 7-fold decrease in the level of
the 
amiloride-sensitive Na+ channel mRNA, one of the
subunits of the amiloride-sensitive Na+ channel, and an
increase in CFTR mRNA. Our data suggest that IL-4 may favor the
hydration of the airway surface by decreasing Na+
absorption and increasing Cl- secretion. This could be
required to fluidify the mucus, which is hypersecreted during
inflammatory conditions. On the other hand, the modifications of ion
transport could also affect the ion composition of airway surface
fluid.
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