| Atopic asthmatic subjects but not atopic subjects without asthma have enhanced inflammatory response to ozone. | |
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MedLine Citation:
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PMID: 20816188 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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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Authors:
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Michelle L Hernandez; John C Lay; Bradford Harris; Charles R Esther; W June Brickey; Philip A Bromberg; David Diaz-Sanchez; Robert B Devlin; Steven R Kleeberger; Neil E Alexis; David B Peden |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S. |
Journal Detail:
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Title: The Journal of allergy and clinical immunology Volume: 126 ISSN: 1097-6825 ISO Abbreviation: J. Allergy Clin. Immunol. Publication Date: 2010 Sep |
Date Detail:
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Created Date: 2010-09-06 Completed Date: 2010-09-28 Revised Date: 2011-09-13 |
Medline Journal Info:
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Nlm Unique ID: 1275002 Medline TA: J Allergy Clin Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 537-44.e1 Citation Subset: AIM; IM |
Copyright Information:
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Published by Mosby, Inc. |
Affiliation:
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Center for Environmental Medicine Asthma and Lung Biology, University of North Carolina School of Medicine, University of North Carolina at Chapel Hill, NC 27599-7310, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adult Asthma / immunology, physiopathology* Female Flow Cytometry Humans Hypersensitivity, Immediate / complications*, physiopathology Inflammation / chemically induced, physiopathology Leukocytes, Mononuclear / cytology, immunology Male Ozone / pharmacology* Respiratory Function Tests Young Adult |
| Grant Support | |
ID/Acronym/Agency:
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KL2 RR025746-04/RR/NCRR NIH HHS; KL2RR025746/RR/NCRR NIH HHS; M01 RR000046-48/RR/NCRR NIH HHS; M01RR00046/RR/NCRR NIH HHS; P01 AT002620-01/AT/NCCAM NIH HHS; P01 AT002620-05/AT/NCCAM NIH HHS; P01AT002620/AT/NCCAM NIH HHS; P30 ES010126-10/ES/NIEHS NIH HHS; P30ES010126/ES/NIEHS NIH HHS; R01 ES012706-05/ES/NIEHS NIH HHS; R01ES012706/ES/NIEHS NIH HHS; U19 AI077437-01/AI/NIAID NIH HHS; U19 AI077437-010003/AI/NIAID NIH HHS; U19AI077437/AI/NIAID NIH HHS; UL1 RR025747-01/RR/NCRR NIH HHS; UL1RR025747/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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10028-15-6/Ozone |
| Comments/Corrections | |
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