Journal
CLINICAL IMMUNOLOGY
Volume 107, Issue 1, Pages 10-19Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/S1521-6616(03)00004-4
Keywords
human basophils; polycyclic aromatic hydrocarbons
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Funding
- NIEHS NIH HHS [R01 ES 05495, P20 ES 09871] Funding Source: Medline
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Polycyclic aromatic hydrocarbons (PAHs) are major components of diesel exhaust particles found in pollutant respirable particles. There is growing evidence that these fossil fuel combustion products exacerbate allergic inflammation. Basophils contribute to allergic inflammation through the release of preformed and granule-derived mediators. To determine whether allergens and PAHs interact, we incubated human basophils with PAHs and measured the release of histamine and IL-4 with and without added antigen. None of the PAHs induced mediator release by itself and none affected total cellular histamine levels. However, several PAHs enhanced histamine release and IL-4 production in response to crosslinking the high-affinity IgE receptor, FcepsilonRI. The enhancement seen with 1,6-BaP-quinone involved an increase in tyrosine phosphorylation in several different substrates, including the FcepsilonRI-associated tyrosine kinase, Lyn, and elevated reactive oxygen species (ROS) levels detected by dichlorofluorescein fluorescence and flow cytometry. The PAH-induced enhancement of mediator release and ROS production could be inhibited with the antioxidant N-acetylcysteine. These data provide further evidence that environmental pollutants can influence allergic inflammation through enhanced FcepsilonRI-coupled mediator release from human basophils. (C) 2003 Elsevier Science (USA). All rights reserved.
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