Skip Navigation



ToxSci Advance Access published online on March 16, 2005
Toxicological Sciences, doi:10.1093/toxsci/kfi141
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
85/2/990    most recent
kfi141v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Jaspers, I.
Right arrow Articles by Madden, M. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jaspers, I.
Right arrow Articles by Madden, M. C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Toxicological Sciences © The Author 2005. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Received January 6, 2005
Accepted March 3, 2005

Respiratory Toxicology

Diesel Exhaust Enhances Influenza Virus Infections in Respiratory Epithelial Cells

Ilona Jaspers 1*, Jonathan M. Ciencewicki 2, Wenli Zhang 3, Luisa E. Brighton 3, Johnny L. Carson 4, Melinda A. Beck 5, and Michael C. Madden 6

1 Center for Environmental Medicine, Asthma, and Lung Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599; Curriculum of Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599; Department of Pediatrics, Division of Infectious Diseases and Host Defense, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599
2 Curriculum of Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599
3 Center for Environmental Medicine, Asthma, and Lung Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599
4 Center for Environmental Medicine, Asthma, and Lung Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599; Department of Pediatrics, Division of Infectious Diseases and Host Defense, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599
5 Department of Pediatrics, Division of Infectious Diseases and Host Defense, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599
6 Curriculum of Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599; U.S. Environmental Protection Agency, Human Studies Division, Chapel Hill, NC 27599

* To whom correspondence should be addressed.
Ilona Jaspers, E-mail: Ilona_Jaspers{at}med.unc.edu


  Abstract

Several factors, such as age and nutritional status can affect the susceptibility to influenza infections. Moreover, exposure to air pollutants, such as diesel exhaust (DE), has been shown to affect respiratory virus infections in rodent models. Influenza virus primarily infects and replicates in respiratory epithelial cells, which are also a major targets for inhaled DE. Using in vitro models of human respiratory epithelial cells, we determined the effects of an aqueous-trapped solution of DE (DEas), on influenza infections. Differentiated human nasal and bronchial epithelial cells, as well as A549 cells, were exposed to DEas and infected with influenza A/Bangkok/1/79. DEas enhanced the susceptibility to influenza virus infection in all cell models, and increased the number of influenza-infected cells within 24 hours post-infection. This was not caused by suppressing antiviral mediator production, since interferon (IFN) {beta} levels, IFN-dependent signaling and IFN-stimulated gene expression was also enhanced by exposure to DEas. Many of the adverse effects induced by DE exposure are mediated by oxidative stress. Exposure to DEE used in these studies generated oxidative stress in respiratory epithelial cells, and addition of the antioxidant glutathione-ethylester (GSH-ET) reversed the effects of DEas on influenza infections. Furthermore, DEas increased influenza virus attachment to respiratory epithelial cells within 2 hours post-infection. Taken together, the results presented here suggest that in human respiratory epithelial cells oxidative stress generated by DEas increases the susceptibility to influenza infection and that exposure to DEas increases the ability of the virus to attach to and enter respiratory epithelial cells.

Keywords: influenza; diesel exhaust; in vitro; epithelial cells; oxidative stress.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Pharmacol. Exp. Ther.Home page
J. P. Buchweitz, P. W. F. Karmaus, J. R. Harkema, K. J. Williams, and N. E. Kaminski
Modulation of Airway Responses to Influenza A/PR/8/34 by {Delta}9-Tetrahydrocannabinol in C57BL/6 Mice
J. Pharmacol. Exp. Ther., November 1, 2007; 323(2): 675 - 683.
[Abstract] [Full Text] [PDF]

Home page
 Toxicol PatholHome page
J. P. Buchweitz, J. R. Harkema, and N. E. Kaminski
Time-Dependent Airway Epithelial and Inflammatory Cell Responses Induced by Influenza Virus A/PR/8/34 in C57BL/6 Mice
Toxicol Pathol, April 1, 2007; 35(3): 424 - 435.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
J. Ciencewicki, L. Brighton, W.-D. Wu, M. Madden, and I. Jaspers
Diesel exhaust enhances virus- and poly(I:C)-induced Toll-like receptor 3 expression and signaling in respiratory epithelial cells
Am J Physiol Lung Cell Mol Physiol, June 1, 2006; 290(6): L1154 - L1163.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.