Traffic‐related air pollution induces non‐allergic eosinophilic airway inflammation and cough hypersensitivity in guinea pigs

Abstract

Background

The pathogenesis and pathophysiology of eosinophilia‐related chronic cough such as non‐asthmatic eosinophilic bronchitis and cough variant asthma are still not clear.

Objective

This study is to examine the potential role of traffic‐related air pollution (TRAP) in eosinophilic inflammation and cough responses.

Methods

Non‐sensitized guinea pigs were exposed to TRAP in an urban traffic tunnel or kept in a filtered air environment for 7 or 14 days. Reflexive cough was measured using citric acid and allyl isothiocyanate (AITC) challenges, respectively. Spontaneous cough counting was determined using audio recording and a waveform analysis. Airway inflammation was evaluated using differential cells in bronchoalveolar lavage fluid (BALF) and lung histopathology. To further elucidate the relationship between airway inflammation and cough hypersensitivity, a subgroup of those exposed for 14 days received a dexamethasone treatment.

Results

Compared to reflexive cough count (mean (95% confidence interval) in 10 min) provoked by the AITC challenge for the unexposed animals (3.1 (1.7‐4.5)), those were increased significantly following both the 7‐day (12.0 (6.8‐17.2), p<0.01) and the 14‐day (12.0 (6.4‐17.6), p<0.01) TRAP exposure. The effect provoked by the citric acid challenge was more profound following the 14‐day exposure (26.0 (19.5‐32.5) vs. 3.8 (1.5‐6.0) for the control, p<0.001). TRAP exposures enhanced spontaneous cough events, caused a significant increase of eosinophils and neutrophils in BALF, and resulted in a dramatic eosinophilic infiltration in submucosal layer of trachea and bronchus, which can be inhibited significantly by dexamethasone treatment.

Conclusions & Clinical Relevance

TRAP exposures induced cough hypersensitivity and non‐allergic eosinophilic inflammation of airways in guinea pigs. This study highlights the potential mechanisms of eosinophilia‐related chronic cough that can be induced by traffic‐related air pollution.

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