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Ozone inhalation induces exacerbation of eosinophilic airway inflammation and hyperresponsiveness in allergen-sensitized mice

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Background: 

Ozone (O3) exposure evokes asthma exacerbations by mechanisms that are poorly understood. We used a murine model to characterize the effects of O3 on allergic airway inflammation and hyperresponsiveness and to identify factors that might contribute to the O3-induced exacerbation of asthma. Methods: 

BALB/c mice were sensitized and challenged with Aspergillus fumigatus (Af). A group of sensitized and challenged mice was exposed to 3.0 ppm of O3 for 2 h and studied 12 h later (96 h after Af challenge). Naive mice and mice exposed to O3 alone were used as controls. Bronchoalveolar lavage (BAL) cellular and cytokine content, lung function [enhanced pause (Penh)], isometric force generation by tracheal rings and gene and protein expression of Fas and FasL were assessed. Apoptosis of eosinophils was quantified by FACS. Results: 

In sensitized mice allergen challenge induced a significant increase of Penh and contractile force in tracheal rings that peaked 24 h after challenge and resolved by 96 h. O3 inhalation induced an exacerbation of airway hyperresponsiveness accompanied by recurrence of neutrophils and enhancement of eosinophils 96 h after allergen challenge. The combination of allergen and O3 exposure inhibited Fas and FasL gene and protein expression and eosinophil apoptosis and increased interleukin-5 (IL-5), granulocyte-macrophage-colony stimulating factor (GM-CSF) and G-CSF protein levels. Conclusions: 

O3 affects airway responsiveness of allergen-primed airways indirectly by increasing viability of eosinophils and eosinophil-mediated pathological changes.
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Keywords: apoptosis; asthma; eosinophils; murine models; ozone

Document Type: Research Article

Affiliations: 1: Pulmonary, Allergy and Critical Care Division, Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA 2: Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA, USA 3: GlaxoSmithKline, King of Prussia, PA, USA

Publication date: 01 April 2008

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