Signature current of SO2-induced bronchitis in rabbit

Nobuhisa Iwase, Tsukasa Sasaki, Sanae Shimura, Toshiaki Fushimi, Hiroshi Okayama, Hiroki Hoshi, Toshiya Irokawa, Kan Sasamori, Koichi Takahashi, Kunio Shirato

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To investigate abnormalities of airway epithelial ion transport underlying chronic inflammatory airway diseases, we performed electrophysiological, histological, and molecular biological experiments using rabbits exposed to SO2 as a model of bronchitis. By comparison with control, the SO2-exposed trachea exhibited decreased short circuit current (Isc) and conductance associated with increased potential difference. In normal trachea, apical ATP induced a transient Isc activation followed by a suppression, whereas the bronchitis model exhibited a prolonged activation without suppression. This pathological ATP response was abolished by diphenylamine 2-carboxylate or Cl- free bath solution. A significant increase in net Cl- flux toward the lumen was observed after ATP in our bronchitis model. Isoproterenol or adenosine evoked a sustained Isc increase in SO2-exposed, but not in normal, tracheas. The Northern blot analysis showed a strong expression of cystic fibrosis transmembrane conductance regulator (CFTR) mRNA in SO2-exposed epithelium. The immunohistochemical study revealed a positive label of CFTR on cells located luminally only in SO2-exposed rabbits. We concluded that the prolonged ATP response in our bronchitis model was of a superimposed normal and adenosine-activated current. The latter current was also activated by isoproterenol and appeared as a signature current for the bronchitis model airway. This was likely mediated by CFTR expressed in the course of chronic inflammation.

Original languageEnglish
Pages (from-to)1651-1661
Number of pages11
JournalJournal of Clinical Investigation
Issue number7
Publication statusPublished - 1997 Apr 1


  • ATP
  • airway epithelium
  • bronchitis
  • cystic fibrosis transmembrane conductance regulator
  • ion transport


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