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Damage‐associated molecular pattern and innate cytokine release in the airways of competitive swimmers
Author(s) -
Seys S. F.,
Hox V.,
Van Gerven L.,
Dilissen E.,
Marijsse G.,
Peeters E.,
Dekimpe E.,
Kasran A.,
Aertgeerts S.,
Troosters T.,
Vanbelle V.,
Peers K.,
Ceuppens J. L.,
Hellings P. W.,
Dupont L. J.,
Bullens D. M.
Publication year - 2015
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/all.12540
Subject(s) - sputum , medicine , airway , immunology , asthma , athletes , innate immune system , physical therapy , pathology , immune system , surgery , tuberculosis
Background Daily intensive exercise by elite athletes can result in exercise‐induced asthma especially in elite swimmers and this may be linked to epithelial damage. Objective To study airway epithelial damage and release of damage‐associated molecular patterns ( DAMP s) after intensive exercise in elite athletes and controls. Methods We recruited competitive swimmers ( n = 26), competitive indoor athletes ( n = 13) and controls ( n = 15) without any history of asthma. Lung function was measured before, immediately after and 24 h after a 90‐min intensive exercise protocol. Sputum induction was performed at baseline and 24 h after exercise. Exercise‐induced bronchoconstriction ( EIB ) was assessed by the eucapnic voluntary hyperventilation test. Results Baseline sputum uric acid, high mobility group box‐1, CXCL8 mRNA , sputum neutrophils and serum Clara cell protein‐16 (CC‐16) were significantly higher in competitive swimmers compared with controls. Intensive swimming for 90 min resulted in an increase of sputum IL‐1β, IL‐6 and TNF mRNA in competitive swimmers, and of sputum IL‐6 mRNA and sputum neutrophils in controls. Although all participants were asymptomatic, seven competitive swimmers, one indoor athlete and one control met the criteria for EIB. Conclusion Our findings show that the intensive training combined with exposure to by‐products of chlorination induces airway epithelial damage in competitive swimmers. This is associated with increased damage‐associated molecular patterns, innate cytokine release and neutrophilic airway inflammation.