The role of chemokines in exercise-induced bronchoconstriction in asthma.
BACKGROUND
The pathogenesis of exercise-induced bronchoconstriction in asthma is incompletely understood, and the role of chemokines has not been investigated.


OBJECTIVE
To investigate the involvement of the CC chemokines eotaxin, regulated upon activation normal T-cell expressed and secreted (RANTES), thymus and activation-regulated chemokine (TARC), and the CXC chemokine interferon-gamma-inducible protein 10 (IP-10) in exercise-induced bronchoconstriction.


METHODS
Four groups were enrolled: asthmatic children with positive (n = 15) and negative (n = 15) responses to exercise, children with cystic fibrosis (n = 14), and healthy children (n = 11). Levels of eotaxin, RANTES, TARC, and IP-10 were determined in plasma before, immediately after, and 6 and 24 hours after exercise challenge using enzyme-linked immunosorbent assay. Transcriptional activity was measured using reverse transcriptase-polymerase chain reaction.


RESULTS
Exercise did not induce any significant changes in systemic chemokine levels. A significant difference was observed only in the preexercise IP-10 levels among groups (P = .045). There was a significant difference in peripheral blood eosinophil counts among groups (P = .003). In asthmatic children with a positive response to exercise, there was an inverse correlation between eosinophil counts and eotaxin levels (r = -0.616; P = .01) and between forced expiratory volume in 1 second and TARC levels (r = -0.865; P = .001). Reverse transcriptase-polymerase chain reaction studies did not show any difference in the transcription of the chemokines.


CONCLUSIONS
Exercise does not cause any changes in the systemic expression of eosinophilic chemokines. Peripheral blood eosinophils may be a determinant of the exercise response, and eotaxin and TARC may be associated with eosinophil counts and forced expiratory volume in 1 second in children with a bronchoconstrictor response to exercise.
Tahan
Fulya
F
Pediatric Allergy and Asthma Unit, Hacettepe University School of Medicine, Hacettepe, Ankara, Turkey.
Karaaslan
Cagatay
C
Aslan
Ayse
A
Kiper
Nural
N
Kalayci
Omer
O
D001249:Asthma / Q000097:blood / Q000276:immunology / Q000378:metabolism*; D016084:Bronchoconstriction; D054413:Chemokine CCL11; D054414:Chemokine CCL17; D018946:Chemokine CCL5 / Q000097:blood; D019742:Chemokines, CC / Q000097:blood / Q000276:immunology / Q000378:metabolism*; D002648:Child; D003550:Cystic Fibrosis / Q000097:blood / Q000378:metabolism; D004804:Eosinophils / Q000378:metabolism; D015444:Exercise / Q000502:physiology*; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007958:Leukocyte Count; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male
C515456:CCL11 protein, human; C106230:CCL17 protein, human; D054413:Chemokine CCL11; D054414:Chemokine CCL17; D018946:Chemokine CCL5; D019742:Chemokines, CC; D007073:Immunoglobulin E