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Research Article Free access | 10.1172/JCI2357

Inducible nitric oxide synthase expression is reduced in cystic fibrosis murine and human airway epithelial cells.

T J Kelley and M L Drumm

Department of Pediatrics, Case Western Reserve University, 8th Floor BRB, 10900 Euclid Avenue, Cleveland, Ohio 44106-4948, USA.

Find articles by Kelley, T. in: JCI | PubMed | Google Scholar

Department of Pediatrics, Case Western Reserve University, 8th Floor BRB, 10900 Euclid Avenue, Cleveland, Ohio 44106-4948, USA.

Find articles by Drumm, M. in: JCI | PubMed | Google Scholar

Published September 15, 1998 - More info

Published in Volume 102, Issue 6 on September 15, 1998
J Clin Invest. 1998;102(6):1200–1207. https://doi.org/10.1172/JCI2357.
© 1998 The American Society for Clinical Investigation
Published September 15, 1998 - Version history
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Abstract

It has been reported that exhaled nitric oxide levels are reduced in cystic fibrosis (CF) patients. We have examined the inducible isoform of nitric oxide synthase (iNOS) in the airways by immunostaining and found that iNOS is constitutively expressed in the airway epithelia of non-CF mouse and human tissues but essentially absent in the epithelium of CF airways. We explored potential consequences of lost iNOS expression and found that iNOS inhibition significantly increases mouse nasal trans-epithelial potential difference, and hindered the ability of excised mouse lungs to prevent growth of Pseudomonas aeruginosa. The absence of continuous nitric oxide production in epithelial cells of CF airways may play a role in two CF-associated characteristics: hyperabsorption of sodium and susceptibility to bacterial infections.

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