The role of lipoxin A4 in exercise-induced bronchoconstriction in asthma
JOURNAL OF ASTHMA, cilt.45, sa.2, ss.161-164, 2008 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 45 Sayı: 2
- Basım Tarihi: 2008
- Doi Numarası: 10.1080/02770900701847068
- Dergi Adı: JOURNAL OF ASTHMA
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.161-164
- Anahtar Kelimeler: asthma, bronchoconstriction, exercise, lipoxin A4, BRONCHIAL HYPERRESPONSIVENESS, AIRWAY HYPERRESPONSIVENESS, A(4), INFLAMMATION, NEUTROPHILS
- Erciyes Üniversitesi Adresli: Evet
Özet
Background. The pathogenesis of exercise-induced bronchoconstriction in asthma is incompletely understood, and the role of lipoxin A4 has not been investigated. Objective. To investigate the involvement of lipoxin A4 in exercise-induced bronchoconstriction. Methods. Two groups of children were enrolled in the study: asthmatic children with positive (n = 12) and negative (n = 8) responses to exercise. Levels of lipoxin A4 were determined in plasma before and immediately after exercise challenge using enzyme-linked immunosorbent assay. Results. No significant difference was observed in the pre-exercise lipoxin A4 levels among the groups (p 0.05). A significant difference was observed in the postexercise lipoxin A4 levels between the two groups (p = 0.041). We also observed significant decreases in plasma lipoxin A4 levels immediately after exercise challenge both in asthmatic children with positive responses to exercise (p = 0.013) and negative responses to exercise (p = 0.05). But these levels were significantly higher in asthmatic children with negative responses to exercise (p = 0.041). There was an inverse correlation between lipoxin A4 levels and a reduction in forced expiratory volume at one second percent after exercise (p = 0.045, r = -0.465). Conclusion. Our results are the first demonstration of the lower levels of lipoxin A4 associated with exercise-induced bronchoconstriction in asthma. We hypothesize that the development of exercise-induced bronchoconstriction in asthmatic children may be in relation to a reduced endogenous lipoxin biosynthetic capability. Lipoxin mimetics and related compounds could provide novel therapeutic approaches to the treatment of exercise-induced bronchoconstriction in asthma.