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Author Notes:

E-mail: Gurjit.Hershey@cchmc.org

Conceived and designed the experiments: GKKH. Performed the experiments: GBL EBB AMG CX. Analyzed the data: GBL EBB CX GKKH.

Contributed reagents/materials/analysis tools: GBL EBB CX TDLC LASB AMF. Wrote the paper: GBL EBB CX GKKH.

We would like to thank M. Ian Gilmour for kindly providing the diesel exhaust particles used in this study and Drs. Melinda Butsch Kovacic, Amal Assa’ad, and Carolyn Kercsmar for helpful discussions about this project.

The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

The authors have declared that no competing interests exist.


Research Funding:

This work was supported by National Institutes of Health (NIH) 1R01HL098134-01 (GKKH and TDLC) and National Institute of Environmental Health Sciences (NIEHS) T32 ES010957 (EBB).


  • Science & Technology
  • Multidisciplinary Sciences
  • Science & Technology - Other Topics
  • MICE

Diesel Exhaust Particles Induce Cysteine Oxidation and S-Glutathionylation in House Dust Mite Induced Murine Asthma


Journal Title:



Volume 8, Number 3


, Pages e60632-e60632

Type of Work:

Article | Final Publisher PDF


Background: Diesel exhaust particle (DEP) exposure enhances allergic inflammation and has been linked to the incidence of asthma. Oxidative stress on the thiol molecules cysteine (Cys) and glutathione (GSH) can promote inflammatory host responses. The effect of DEP on the thiol oxidation/reduction (redox) state in the asthmatic lung is unknown. Objective: To determine if DEP exposure alters the Cys or GSH redox state in the asthmatic airway. Methods: Bronchoalveolar lavage fluid was obtained from a house dust mite (HDM) induced murine asthma model exposed to DEP. GSH, glutathione disulfide (GSSG), Cys, cystine (CySS), and s-glutathionylated cysteine (CySSG) were determined by high pressure liquid chromatography. Results: DEP co-administered with HDM, but not DEP or HDM alone, decreased total Cys, increased CySS, and increased CySSG without significantly altering GSH or GSSG. Conclusions: DEP exposure promotes oxidation and S-glutathionylation of cysteine amino acids in the asthmatic airway, suggesting a novel mechanism by which DEP may enhance allergic inflammatory responses. © 2013 Lee et al.

Copyright information:

2013 Lee et al.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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