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Effect of preexposure to ultrafine carbon black on respiratory syncytial virus infection in mice.

Publication ,  Journal Article
Lambert, AL; Trasti, FS; Mangum, JB; Everitt, JI
Published in: Toxicol Sci
April 2003

Epidemiological studies have indicated that exposure to elevated levels of particulate matter exacerbates several pulmonary diseases, including asthma, bronchitis, and viral infections. Respiratory syncytial virus (RSV) is the major cause of bronchiolitis and pneumonia in infants and may lead to the development of asthma in childhood. To determine whether particle exposure modulates the immune response to RSV, eight-week-old female BALB/c mice received an intratracheal (i.t.) instillation of either 40 micro g ultrafine carbon black (CB) particles or vehicle. The following day, mice were i.t. instilled with either 106 pfu RSV or uninfected media. End points were examined 1, 2, 4, 7, and 10 days during RSV infection. Compared with RSV alone, tumor necrosis factor-alpha (TNF-alpha) protein was reduced in the bronchoalveolar lavage fluid (BALF) on days 1 and 2 of infection; there was also a reduction in BALF lymphocyte numbers on day 4, which correlated with reductions in both IFN-gamma-inducible protein (IP-10), lymphotactin, and IFN-gamma mRNAs in the lungs of RSV + CB mice. Multiprobe ribonuclease protection assays of RSV + CB lung tissue showed no changes in the RSV-associated chemokines regulated upon activation, normal T cell expressed and secreted (RANTES), eotaxin, monocyte chemoattractant protein (MCP-1), macrophage inflammatory protein (MIP)-1 alpha or MIP-1 beta. Viral titers in RSV + CB mice were lower than RSV on days 2-4 of infection. By day 7 of infection, however, neutrophil numbers, proinflammatory cytokine mRNA expression, and protein levels of TNF-alpha and the Th2 cytokine interleukin (IL)-13 were increased in the lungs of RSV + CB mice, indicating an exacerbation of infection. These data indicate that preexposure to ultrafine particles induces an inflammatory milieu promoting allergic immune responses rather than IFNgamma production necessary for microbial defense.

Duke Scholars

Published In

Toxicol Sci

DOI

ISSN

1096-6080

Publication Date

April 2003

Volume

72

Issue

2

Start / End Page

331 / 338

Location

United States

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Toxicology
  • Specific Pathogen-Free Organisms
  • Respiratory Syncytial Viruses
  • Respiratory Syncytial Virus Infections
  • RNA, Messenger
  • Particle Size
  • Mice, Inbred BALB C
  • Mice
  • Lung
 

Citation

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MLA
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Lambert, A. L., Trasti, F. S., Mangum, J. B., & Everitt, J. I. (2003). Effect of preexposure to ultrafine carbon black on respiratory syncytial virus infection in mice. Toxicol Sci, 72(2), 331–338. https://doi.org/10.1093/toxsci/kfg031
Lambert, Amy L., Frances S. Trasti, James B. Mangum, and Jeffrey I. Everitt. “Effect of preexposure to ultrafine carbon black on respiratory syncytial virus infection in mice.Toxicol Sci 72, no. 2 (April 2003): 331–38. https://doi.org/10.1093/toxsci/kfg031.
Lambert AL, Trasti FS, Mangum JB, Everitt JI. Effect of preexposure to ultrafine carbon black on respiratory syncytial virus infection in mice. Toxicol Sci. 2003 Apr;72(2):331–8.
Lambert, Amy L., et al. “Effect of preexposure to ultrafine carbon black on respiratory syncytial virus infection in mice.Toxicol Sci, vol. 72, no. 2, Apr. 2003, pp. 331–38. Pubmed, doi:10.1093/toxsci/kfg031.
Lambert AL, Trasti FS, Mangum JB, Everitt JI. Effect of preexposure to ultrafine carbon black on respiratory syncytial virus infection in mice. Toxicol Sci. 2003 Apr;72(2):331–338.
Journal cover image

Published In

Toxicol Sci

DOI

ISSN

1096-6080

Publication Date

April 2003

Volume

72

Issue

2

Start / End Page

331 / 338

Location

United States

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Toxicology
  • Specific Pathogen-Free Organisms
  • Respiratory Syncytial Viruses
  • Respiratory Syncytial Virus Infections
  • RNA, Messenger
  • Particle Size
  • Mice, Inbred BALB C
  • Mice
  • Lung