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. 2010 Sep;126(3):537-44.e1.
doi: 10.1016/j.jaci.2010.06.043.

Atopic asthmatic subjects but not atopic subjects without asthma have enhanced inflammatory response to ozone

Michelle L Hernandez  1 , John C Lay, Bradford Harris, Charles R Esther Jr, W June Brickey, Philip A Bromberg, David Diaz-Sanchez, Robert B Devlin, Steven R Kleeberger, Neil E Alexis, David B Peden
Affiliations

Atopic asthmatic subjects but not atopic subjects without asthma have enhanced inflammatory response to ozone

Michelle L Hernandez et al. J Allergy Clin Immunol. 2010 Sep.

Abstract

Background: Asthma is a known risk factor for acute ozone-associated respiratory disease. Ozone causes an immediate decrease in lung function and increased airway inflammation. The role of atopy and asthma in modulation of ozone-induced inflammation has not been determined.

Objective: We sought to determine whether atopic status modulates ozone response phenotypes in human subjects.

Methods: Fifty volunteers (25 healthy volunteers, 14 atopic nonasthmatic subjects, and 11 atopic asthmatic subjects not requiring maintenance therapy) underwent a 0.4-ppm ozone exposure protocol. Ozone response was determined based on changes in lung function and induced sputum composition, including airway inflammatory cell concentration, cell-surface markers, and cytokine and hyaluronic acid concentrations.

Results: All cohorts experienced similar decreases in lung function after ozone. Atopic and atopic asthmatic subjects had increased sputum neutrophil numbers and IL-8 levels after ozone exposure; values did not significantly change in healthy volunteers. After ozone exposure, atopic asthmatic subjects had significantly increased sputum IL-6 and IL-1beta levels and airway macrophage Toll-like receptor 4, Fc(epsilon)RI, and CD23 expression; values in healthy volunteers and atopic nonasthmatic subjects showed no significant change. Atopic asthmatic subjects had significantly decreased IL-10 levels at baseline compared with healthy volunteers; IL-10 levels did not significantly change in any group with ozone. All groups had similar levels of hyaluronic acid at baseline, with increased levels after ozone exposure in atopic and atopic asthmatic subjects.

Conclusion: Atopic asthmatic subjects have increased airway inflammatory responses to ozone. Increased Toll-like receptor 4 expression suggests a potential pathway through which ozone generates the inflammatory response in allergic asthmatic subjects but not in atopic subjects without asthma.

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Conflict of interest statement

Disclosure of potential conflict of interest: B. Harris has received research support from the National Institute of Environmental Health Sciences, the US Environmental Protection Agency, and Purdue Pharmaceuticals–Quintiles. P. A. Bromberg has received research support from the US Environmental Protection Agency and the National Institutes of Health. D. B. Peden has consulted for GlaxoSmithKline and Funxional Therapeutics and has received research support from the National Institute of Environmental Health Sciences; the National Institute for Allergy and Infectious Diseases; the National Center for Complementary and Alternative Medicine; the National Heart, Lung, and Blood Institute; the US Environmental Protection Agency; the National Center for Research Resources. The rest of the authors have declared that they have no conflict of interest.

Figures

Figure 1
Figure 1
Baseline and post O3 exposure FEV1 (A) and FVC (B). n=25 normal volunteers (NV), 13 atopics, and 11 atopic asthmatics (AA). Data bars depict mean and standard error of the mean.
Figure 2
Figure 2
Changes in inflammatory cell infiltrate in sputum (cells/mg sputum) in response to O3. N=25 normal volunteers, 13 atopics, and 10 AA. Lines depict mean and standard error of the mean.
Figure 3
Figure 3
Changes in induced sputum cytokines and hyaluronic acid (HA) in response to O3. N=24 NV, 12 atopics, and 10 AA for sputum cytokines, N=10 each cohort for HA measurement in sputum. Lines depict mean and standard error of the mean.
Figure 4
Figure 4
Changes in cell surface marker expression (MFI) on induced sputum macrophages. N=13 normal volunteers (NV), 7 atopics, and 6 atopic asthmatics. Lines depict mean and standard error of the mean.
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References

    1. Peden D. Air Pollution: Indoor and Outdoor. In: Adkinson NF Jr, Busse W, Bochner B, Holgate S, Simons FE, Lemanske R, editors. MIDDLETON'S ALLERGY: PRINCIPLES AND PRACTICE. 7 ed ed. Mosby: 2008. pp. 495–508.
    1. Bernstein JA, Alexis N, Barnes C, Bernstein IL, Nel A, Peden D, et al. Health effects of air pollution. J Allergy Clin Immunol. 2004;114:1116–1123. - PubMed
    1. Peden DB. The epidemiology and genetics of asthma risk associated with air pollution. J Allergy Clin Immunol. 2005;115:213–219. quiz 20. - PubMed
    1. Peden DB, Boehlecke B, Horstman D, Devlin R. Prolonged acute exposure to 0.16 ppm ozone induces eosinophilic airway inflammation in asthmatic subjects with allergies. J Allergy Clin Immunol. 1997;100:802–808. - PubMed
    1. Kehrl HR, Peden DB, Ball B, Folinsbee LJ, Horstman D. Increased specific airway reactivity of persons with mild allergic asthma after 7.6 hours of exposure to 0.16 ppm ozone. J Allergy Clin Immunol. 1999;104:1198–1204. - PubMed

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