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Biomarkers

High Serum Arginase I Levels in Asthma: its Correlation with High-Sensitivity C-Reactive Protein

, M.D., Ph.D., , M.D., Ph.D., , M.T., , M.D., , M.D., Ph.D., , M.D., Ph.D., , M.D., Ph.D. & , M.D., Ph.D. show all
Pages 1-7 | Published online: 01 Nov 2010
 

Abstract

Background. Much attention has been directed to the induction of arginase I in the lung of asthmatic mice. However, there is no agreement on the changes of serum arginase activity in asthmatic patients among previous studies. Objectives. The aim of this study was to evaluate the clinical relevance of serum arginase I in asthmatic patients. Methods. Serum arginase I was examined cross-sectionally in non-smoking asthmatic patients (n = 23) and healthy individuals (n = 30) using enzyme-linked immunosorbent assay (ELISA) and its correlations with several clinical parameters were investigated. Results. Serum levels of arginase I were significantly increased in asthmatic patients (mean ± SD 67.4 ± 41.0 ng/mL) compared with healthy controls (27.2 ± 12.9 ng/mL). In healthy controls, a difference in arginase I levels was not observed between sex groups but was observed between age groups. In asthmatic patients, serum arginase I levels were not different between groups of age, sex, and inhalation steroid therapy but were different between groups of atopic status. Non-atopic asthmatic patients revealed significantly high serum arginase I levels compared with atopic asthmatic patients and healthy controls although no difference was observed between atopic asthmatic patients and healthy controls. Spearman's correlation analysis showed that serum arginase I level had a significant negative correlation with age and a positive correlation with red blood cell numbers in healthy controls, whereas in asthmatic patients, it had significant positive correlations with alanine aminotransferase (ALT), high-sensitivity C-reactive protein (hs-CRP) and a negative correlation with immunoglobulin-E (IgE). Conclusions. High serum arginase I levels in asthmatic patients may be associated with airway inflammation in non-atopic asthma.

Acknowledgments

This work was supported in part by Grant-in-Aid for Science Research No. 19390163 from the Ministry of Education, Culture, Sports, Science and Technology of the Japanese Government.

Declaration of Interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.

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