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Airway purinergic responses in healthy, atopic nonasthmatic, and atopic asthmatic subjects exposed to ozone**
Citation:
Esther, C., D. Peden, N. Alexis, AND M. Hernandez. Airway purinergic responses in healthy, atopic nonasthmatic, and atopic asthmatic subjects exposed to ozone**. INHALATION TOXICOLOGY. Taylor & Francis, Inc., Philadelphia, PA, 23(6):324-30, (2011).
Impact/Purpose:
This manuscript was orginally cleared via paper file ephd-12-053 and entered in the science inventory
Description:
Context: Ozone exposure triggers airway inflammatory responses that maybe influenced bybiologically active purine metabolites. Objective:To examinethe relationships between airway purine metabolites and established inflammatory markers of ozone exposure, and to determine if these relationships are altered in individuals with atopyorasthma. Materials and methods: Mass spectrometry was utilized to measure concentrations of purine metabolites (adenosine monophosphate[AMP], adenosine, hypoxanthine,uricacid)and non-purtnemetabolnes(taurine,urea,phenylalanine, tyrosine) in induced sputum obtained from 31 subjects with normal lung function (13 healthy controls, eight atopic nonasthmatics, and 10 atopic asthmatic[AAl] before and 4h after ozone exposure. Results: At baseline, the purines AMP and hypoxanthine correlated with multiple inflammatory markers including neutrophil counts and the cytokines interleukin (IL-6), IL-8, tumor necrosis factor alpha (TNF-a), and IL-1B (r ranged from 0.41 to 0.66, all P<0.05). Following ozone exposure,these purines remained correlated with IL-6,IL-8, and TNF-a (r=0.37-O.68). However, AMP and hypoxanthine Increased significantly post ozone exposure in atopic non asthmatics but not in AA.In contrast, the non-purine metabolite taurine correlated with baseline neutrophil counts (r= 0.56) and IL-6(r=0.53) and was elevated post-exposure in both atopic cohorts. Discussion and conclusions: The purine metabolites AMP and hypoxanthine are correlated with multiple inflammatory markers at baseline and after ozone exposure. However changes in these purine metabolites after ozone appear to differ from other inflammatory markers, with less response in AA relative to atopic nonasthmatics. Purine metabolites may play a role in the signaling responses to ozone, but these responses maybe altered in subjects with asthma.