Skip Navigation



ToxSci Advance Access published online on March 7, 2003
Toxicological Sciences, doi:10.1093/toxsci/kfg032
Toxicological Sciences © Society of Toxicology 2003; all rights reserved
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
72/2/339    most recent
kfg032v1
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 Lambert, A. L.
Right arrow Articles by Everitt, J. I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lambert, A. L.
Right arrow Articles by Everitt, J. I.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Received October 14, 2002; accepted January 2, 2003
© 2003 Society of Toxicology

Respiratory Toxicology

Ultrafine Carbon Black Particles Enhance Respiratory Syncytial Virus-Induced Airway Reactivity, Pulmonary Inflammation and Chemokine Expression

Amy L. Lambert 1*, James B. Mangum 1, Michael P. DeLorme 1, Jeffrey I. Everitt 1

1 CIIT Centers for Health Research, Research Triangle Park, North Carolina, USA

* To whom correspondence should be addressed. E-mail: lambert{at}sri.org.


  Abstract

Exposure to particulate matter (PM) may exacerbate preexisting respiratory diseases such as asthma, chronic obstructive pulmonary disease (COPD), bronchitis, and pneumonia. However, few experimental studies have addressed the effects of PM on lower respiratory tract (LRT) viral infection. Respiratory syncytial virus (RSV) is a major etiological agent for LRT infections in infants, the elderly, and the immunocompromised and may lead to chronic wheezing and the development of asthma in children. In this study, we examined the effects of carbon black (CB) on RSV-induced pulmonary inflammation, chemokine and cytokine expression, and airway hyperresponsiveness in a mouse model of RSV. Female BALB/c mice were instilled via the trachea (i.t.) with 1 x 106 plaque forming units (pfu) RSV or with uninfected culture media. On day 3 of infection, mice were i.t. instilled with either 40 µg ultrafine (CB) particles or with saline. End points were examined on days 4, 5, 7, and 14 of RSV infection. Viral titer and clearance in the lung were unaffected by CB exposure. Neutrophil numbers were elevated on days 4 and 7, and lymphocyte numbers were higher on days 4 and 14 of infection in CB-exposed, RSV-infected mice. CB exposure also enhanced RSV-induced airway hyperresponsiveness to methacholine, BAL total protein, and virus-associated chemokines MCP-1, MIP-1{alpha}, and RANTES. MIP-1{alpha} mRNA expression was increased in the alveolar epithelium, where ultrafine particles deposit in the lung. These data demonstrate a synergistic effect of ultrafine carbon black particles on RSV infection, and suggest a potential mechanism for increased respiratory infections in human populations after PM exposure.

RSV, chemokine, cytokine, ultrafine particles, airway hyperresponsiveness, laser capture microdissection, mouse .


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 EndocrinolHome page
A. L Gruver, M. S Ventevogel, and G. D Sempowski
Leptin receptor is expressed in thymus medulla and leptin protects against thymic remodeling during endotoxemia-induced thymus involution
J. Endocrinol., October 1, 2009; 203(1): 75 - 85.
[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.