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Published ahead of print on September 15, 2005, doi:10.1164/rccm.200502-253OC

Am. J. Respir. Crit. Care Med., Volume 172, Number 12, December 2005, 1523-1528

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Submitted on February 16, 2005
Accepted on September 15, 2005

Increased Arginase Activity in Cystic Fibrosis Airways

Hartmut Grasemann1*, Raphael Schwiertz1, Sonja Matthiesen2, Kurt Racke2, and Felix Ratjen1

1 University of Duisburg-Essen, Children's Hospital, Essen, Germany, 2 University of Bonn, Institute for Pharmacology and Toxicology, Bonn, Germany

* To whom correspondence should be addressed. E-mail: hartmut.grasemann{at}sickkids.ca.

Rationale: Airway nitric oxide concentrations are reduced in cystic fibrosis. Arginases compete for L-arginine, the substrate of nitric oxide synthesis. Objectives: We hypothesized that increased arginase activity may be one factor contributing to nitric oxide deficiency in cystic fibrosis. Measurements: We therefore studied sputum arginase activity, exhaled nitric oxide, and pulmonary function in patients with cystic fibrosis. Results: Mean (± SEM) sputum arginase activity was significantly higher in patients admitted for pulmonary exacerbation compared to patients with stable disease (1.032 ± 0.148 vs. 0.370 ± 0.091 U/mg protein, p = 0.004). Fourteen days of intravenous antibiotic treatment resulted in significant decreased sputum arginase activity in all patients (p = 0.0002). However, arginase activity was still significantly (p = 0.0001) higher in cystic fibrosis sputum after treatment for exacerbation compared to induced sputum from healthy controls (0.026 ± 0.006 U/mg protein). Negative correlations were found for sputum arginase activity at admission with FEV1 (r = -0.41, p = 0.01), as well as changes in arginase activity with percent change in FEV1 during antibiotic therapy (r = - 0.4, p < 0.01) in CF. Exhaled nitric oxide in cystic fibrosis was positively correlated to FEV1 (r = 0.34, p = 0.007), and in patients admitted for pulmonary exacerbation negatively correlated to sputum arginase activity (r = -0.45, p = 0.03). Conclusions: These data suggest that increased sputum arginase activity contributes to nitric oxide deficiency in cystic fibrosis lung disease and may be relevant in the pathogenesis of cystic fibrosis airway disease.
Key words: nitric oxide, inflammatory marker, pulmonary function




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