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Original Article

 

Increased Postexercise Lipoxin A4 Levels in Exhaled Breath Condensate in Asthmatic Children With Exercise-Induced Bronchoconstriction

 

Tahan F1, Eke Gungor H1, Bicici E1, Saraymen B2, Akar HH1

1Department of Pediatric Allergy, School of Medicine, Erciyes University, Kayseri, Turkey
2Department of Biochemistry, School of Medicine, Erciyes University, Kayseri, Turkey

J Investig Allergol Clin Immunol 2016; Vol. 26(1): 19-24
doi: 10.18176/jiaci.0003

 

 Abstract


Background: Lipoxins could be potential modulators of inflammation in the lungs. To our knowledge, the role of exhaled breath condensate (EBC) lipoxin A4 (LXA4) in asthmatic children with exercise-induced bronchoconstriction (EIB) has not been investigated.

Objective: The aim of our study was to determine the involvement of EBC LXA4 in EIB.

Methods: Forty-five patients aged between 5 and 17 years were included in the study. Patients were divided into 2 groups: asthmatic children with a positive response to exercise (n=17) and asthmatic children with a negative response to exercise (n=28). Levels of LXA4 were determined in EBC before and immediately after the exercise challenge using ELISA.

Results: EBC LXA4 levels were significantly increased immediately after exercise in asthmatic children with a positive response to the exercise challenge (P=.05). No significant differences were observed in children with a negative response to exercise (P>.05). There was an inverse correlation between LXA4 levels and the percent degree of reduction in forced expiratory volume in the first second (FEV1%) postexercise in children with a positive exercise challenge (P=.05, r=-0.50). No significant differences were observed in LXA4 levels between atopic and nonatopic asthmatics (P>.05, Mann-Whitney U test).

Conclusions: Levels of EBC LXA4 increased immediately after exercise in asthmatic children with a positive exercise challenge response. We hypothesize that airway LXA4 levels increase to compensate bronchoconstriction and suppress acute inflammation, and that spontaneous bronchodilatation after EIB may be due to LXA4.

Key words: Asthma. Exercise-induced bronchoconstriction. Exhaled breath condensate. Lipoxin A4.