Abstract

BackgroundExercise-induced bronchoconstriction (EIB) is a transient airway narrowing, occurring during or shortly after intensive exercise. It is highly prevalent in non-asthmatic outdoor endurance athletes suggesting an important contribution of air pollution in the development of EIB. Therefore, more research is necessary to investigate the combination of exercise and pollutants on the airways.MethodsBalbc/ByJ mice were intranasally challenged 5 days a week for 3 weeks with saline or 0.2 mg/ml diesel exhaust particles (DEP), prior to a daily incremental running session or non-exercise session. Once a week, the early ventilatory response was measured and lung function was determined at day 24. Airway inflammation and cytokine levels were evaluated in bronchoalveolar lavage fluid. Furthermore, innate lymphoid cells, dendritic cells and tight junction mRNA expression were determined in lung tissue.ResultsSubmaximal exercise resulted in acute alterations of the breathing pattern and significantly improved FEV0.1 at day 24. DEP exposure induced neutrophilic airway inflammation, accompanied with increased percentages of CD11b+ DC in lung tissue and pro-inflammatory cytokines, such as IL-13, MCP-1, GM-CSF and KC. Occludin and claudin-1(Cldn-1) expression were respectively increased and decreased by DEP exposure. Whereas, exercise increased Cldn-3 and Cldn-18 expression. Combining exercise and DEP exposure resulted in significantly increased SP-D levels in the airways.ConclusionDEP exposure induced typical airway neutrophilia, DC recruitment and pro-inflammatory cytokine production. Whereas, intensive exercise induced changes of the breathing pattern. The combination of both triggers resulted in a dysregulation of tight junction expression, suggesting that intensive exercise in polluted environments can induce important changes in the airway physiology and integrity.

Highlights

  • Exercise-induced bronchoconstriction (EIB) is a transient airway narrowing, occurring during or shortly after intensive exercise

  • Ti and Te were significantly increased in both exercise groups after the running session compared with the non-exercise groups at day 22 for Ti and Te of Sal/E mice (p < 0.001 for Ti and p < 0.05 for Te), at day 1 for Ti of diesel exhaust particles (DEP)/E mice (p < 0.05), at day 22 for Te of Sal/E mice (p < 0.05) and at all time points for Te of DEP/E mice compared to the non-exercised control group (p < 0.05 at day 8 and 15, p < 0.01 at day 1 and 22)

  • A significant decrease of PIF post-exercise was seen at day 22 for the Sal/E mice (p < 0.05) and at all time points for DEP exposed mice compared to their non-exercised counterparts (p < 0.05 at day 1, 8 and 15, p < 0.01 at day 22), while the decreased peak expiratory flow (PEF) in exercised mice did not reach significance (Fig. 3d and e, respectively)

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Summary

Introduction

Exercise-induced bronchoconstriction (EIB) is a transient airway narrowing, occurring during or shortly after intensive exercise It is highly prevalent in non-asthmatic outdoor endurance athletes suggesting an important contribution of air pollution in the development of EIB. Similar inflammatory responses were described in elite swimmers; in whom sputum uric acid, high mobility group box-1 and serum CC16 were elevated after 90-min intensive swimming [10]. These epithelial, cellular and biochemical changes were mostly accompanied with increased neutrophilic airway inflammation [1, 5, 9, 10]. It is hypothesised that epithelial injury is a consequence of increased shear stress due to a high ventilation and/or environmental exposures

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