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Adjuvant effects of ambient particulate matter monitored by proteomics of bronchoalveolar lavage fluid

Ambient particulate matter (PM) from air pollution is associated with exacerbation of asthma. The immunological basis for the adjuvant effects of PM is still not well understood. The generation of ROS and the resulting oxidative stress has been identified as one of the major mechanisms. Using a new...

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Bibliographic Details
Published in:Proteomics (Weinheim) 2010-02, Vol.10 (3), p.520-531
Main Authors: Kang, Xuedong, Li, Ning, Wang, Meiying, Boontheung, Pinmanee, Sioutas, Constantinos, Harkema, Jack R, Bramble, Lori A, Nel, Andre E, Loo, Joseph A
Format: Article
Language:English
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Summary:Ambient particulate matter (PM) from air pollution is associated with exacerbation of asthma. The immunological basis for the adjuvant effects of PM is still not well understood. The generation of ROS and the resulting oxidative stress has been identified as one of the major mechanisms. Using a new intranasal sensitization model in which ambient PM is used as an adjuvant to enhance allergic inflammation (Li et al., Environ. Health Perspect. 2009, 117, 1116-1123), a proteomics approach was applied to study the adjuvant effects of ambient PM. The enhanced in vivo adjuvant effect of ultrafine particles correlates with a higher in vitro oxidant potential and a higher content of redox-cycling organic chemicals. Bronchoalveolar lavage fluid proteins from normal and sensitized mice were resolved by 2-DE, and identified by MS. Polymeric immunoglobulin receptor, complement C3, neutrophil gelatinase-associated lipocalin, chitinase 3-like protein 3, chitinase 3-like protein 4, and acidic mammalian chitinase demonstrated significantly enhanced up-regulation by UFP with a polycyclic aromatic hydrocarbon content and a higher oxidant potential. These proteins may be the important specific elements targeted by PM in air pollution through the ability to generate ROS in the immune system, and may be involved in allergen sensitization and asthma pathogenesis.
ISSN:1615-9853
1615-9861
1615-9861
DOI:10.1002/pmic.200900573