Airway inflammation in exercise-induced bronchospasm occurring in athletes without asthma.
Exercise-induced bronchospasm (EIB) occurs in athletes with and without asthma. Studies have suggested an inflammatory basis for EIB in asthmatics; however whether inflammation plays a similar role in EIB in athletes without asthma remains unclear. Our objective was to determine whether there is evidence of an inflammatory basis for exercise-induced bronchospasm occurring in non-asthmatic athletes. Ninety-six athletes without asthma from varsity college teams underwent eucapnic voluntary hyperventilation testing. Sputum was induced from subjects with hypertonic saline inhalation post-eucapnic voluntary hyperventilation testing and was analyzed with enzyme-linked immunosorbent assays for IL-5, IL-8, IL-13, cysteinyl-leukotrienes, prostaglandin E2, histamine, leukotriene B4, and thromboxane B2. In addition, inflammatory (neutrophils, lymphocytes, eosinophils, and macrophages) and epithelial cell counts in sputum were recorded. Multivariate regression modeling showed a significant correlation between concentrations of select inflammatory mediators after eucapnic voluntary hyperventilation testing and severity of EIB. Means of the log-transformed concentrations of inflammatory mediators in EIB-positive athletes were significantly higher post-eucapnic voluntary hyperventilation than in EIB-negative athletes. Similar findings were not demonstrated with inflammatory cells. Concentrations of inflammatory mediators are higher in EIB-positive athletes than in EIB-negative athletes without asthma after eucapnic voluntary hyperventilation testing. The severity of EIB in our cohort also is significantly correlated with increased concentrations of select inflammatory mediators suggesting a potential inflammatory basis for EIB in athletes without asthma.
The Ohio State University Medical Center, Columbus, Ohio, USA.
Jonathan P
JP
Parsons
Christopher P
CP
Baran
Gary
G
Phillips
David
D
Jarjoura
Christopher
C
Kaeding
Benjamin
B
Bringardner
Gail
G
Wadley
Clay B
CB
Marsh
John G
JG
Mastronarde
D000328:Adult; D000367:Age Factors; D001249:Asthma / Q000503:physiopathology; D001250:Asthma, Exercise-Induced / Q000453:epidemiology* / Q000503:physiopathology*; D016535:Bronchial Hyperreactivity / Q000503:physiopathology; D015331:Cohort Studies; D015232:Dinoprostone / Q000032:analysis; D005260:Female; D006632:Histamine / Q000032:analysis; D006801:Humans; D015994:Incidence; D007249:Inflammation / Q000097:blood / Q000503:physiopathology; D018836:Inflammation Mediators / Q000032:analysis*; D007975:Leukotriene B4 / Q000032:analysis; D008297:Male; D015999:Multivariate Analysis; D011336:Probability; D012129:Respiratory Function Tests; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D012737:Sex Factors; D013177:Sports / Q000502:physiology*; D013183:Sputum / Q000378:metabolism*; D013929:Thromboxane B2 / Q000032:analysis
D018836:Inflammation Mediators; D007975:Leukotriene B4; D013929:Thromboxane B2; D006632:Histamine; D015232:Dinoprostone