期刊
ALLERGY
卷 63, 期 4, 页码 438-446出版社
BLACKWELL PUBLISHING
DOI: 10.1111/j.1398-9995.2007.01587.x
关键词
apoptosis; asthma; eosinophils; murine models; ozone
资金
- NHLBI NIH HHS [HL04029, 1R01 HL076646-01, HL080676-01, R01 HL080676, R01 HL076646] Funding Source: Medline
- NIAID NIH HHS [1R01 AI055593-01A1, R01 AI055593] Funding Source: Medline
Background: Ozone (O-3) exposure evokes asthma exacerbations by mechanisms that are poorly understood. We used a murine model to characterize the effects of O-3 on allergic airway inflammation and hyperresponsiveness and to identify factors that might contribute to the O-3-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 O-3 for 2 h and studied 12 h later (96 h after Af challenge). Naive mice and mice exposed to O-3 alone were used as controls. Bronchoalveolar lavage (BAL) cellular and cytokine content, lung function [enhanced pause (P-enh)], 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 P-enh and contractile force in tracheal rings that peaked 24 h after challenge and resolved by 96 h. O-3 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 O-3 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: O-3 affects airway responsiveness of allergen-primed airways indirectly by increasing viability of eosinophils and eosinophil-mediated pathological changes.
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