ToxSci Advance Access originally published online on March 16, 2005
Toxicological Sciences 2005 85(2):990-1002; doi:10.1093/toxsci/kfi141
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Diesel Exhaust Enhances Influenza Virus Infections in Respiratory Epithelial Cells
,
,1,
* Center for Environmental Medicine, Asthma, and Lung Biology; Curriculum of Toxicology; Department of Pediatrics, Division of Infectious Diseases and Host Defense; University of North Carolina at Chapel Hill, North Carolina 27599–7310; and U.S. Environmental Protection Agency, Human Studies Division; Chapel Hill, North Carolina 27599
Received January 6, 2005; accepted March 3, 2005
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 h post-infection. This was not caused by suppressing antiviral mediator production, since interferon (IFN) ß levels, IFN-dependent signaling, and IFN-stimulated gene expression were also enhanced by exposure to DEas. Many of the adverse effects induced by DE exposure are mediated by oxidative stress. Exposure to DEas 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 h 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.
Key Words: influenza; diesel exhaust; in vitro; epithelial cells; oxidative stress.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  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]
|
|
|
|
 |
|
 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]
|
|
|
|
 |
|
 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]
|
|