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Research Article Free access | 10.1172/JCI119328

Signature current of SO2-induced bronchitis in rabbit.

N Iwase, T Sasaki, S Shimura, T Fushimi, H Okayama, H Hoshi, T Irokawa, K Sasamori, K Takahashi, and K Shirato

First Department of Internal Medicine, Tohoku University School of Medicine, Aoba-ku, Sendai, Japan.

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First Department of Internal Medicine, Tohoku University School of Medicine, Aoba-ku, Sendai, Japan.

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First Department of Internal Medicine, Tohoku University School of Medicine, Aoba-ku, Sendai, Japan.

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First Department of Internal Medicine, Tohoku University School of Medicine, Aoba-ku, Sendai, Japan.

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First Department of Internal Medicine, Tohoku University School of Medicine, Aoba-ku, Sendai, Japan.

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First Department of Internal Medicine, Tohoku University School of Medicine, Aoba-ku, Sendai, Japan.

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First Department of Internal Medicine, Tohoku University School of Medicine, Aoba-ku, Sendai, Japan.

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First Department of Internal Medicine, Tohoku University School of Medicine, Aoba-ku, Sendai, Japan.

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First Department of Internal Medicine, Tohoku University School of Medicine, Aoba-ku, Sendai, Japan.

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First Department of Internal Medicine, Tohoku University School of Medicine, Aoba-ku, Sendai, Japan.

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Published April 1, 1997 - More info

Published in Volume 99, Issue 7 on April 1, 1997
J Clin Invest. 1997;99(7):1651–1661. https://doi.org/10.1172/JCI119328.
© 1997 The American Society for Clinical Investigation
Published April 1, 1997 - Version history
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Abstract

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.

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