Cytokine expression in mice exposed to diesel exhaust particles by inhalation. Role of tumor necrosis factor

Research output: Research - peer-reviewJournal article – Annual report year: 2006

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  • Author: Saber, Anne T

    National Research Centre for the Working Environment

  • Author: Jacobsen, Nicklas R.

    National Research Centre for the Working Environment

  • Author: Bornholdt, Jette

    National Research Centre for the Working Environment

  • Author: Kjær, Sanna L.

    National Research Centre for the Working Environment

  • Author: Dybdahl, Marianne

    National Research Centre for the Working Environment

  • Author: Risom, Lotte

    University of Copenhagen

  • Author: Loft, Steffen

    University of Copenhagen

  • Author: Vogel, Ulla

    National Research Centre for the Working Environment

  • Author: Wallin, Håkan

    National Research Centre for the Working Environment

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Background: Particulate air pollution has been associated with lung and cardiovascular disease, for which lung inflammation may be a driving mechanism. The pro-inflammatory cytokine, tumor necrosis factor (TNF) has been suggested to have a key-role in particle-induced inflammation. We studied the time course of gene expression of inflammatory markers in the lungs of wild type mice and Tnf-/-mice after exposure to diesel exhaust particles (DEPs). Mice were exposed to either a single or multiple doses of DEP by inhalation. We measured the mRNA level of the cytokines Tnf and interleukin-6 (Il-6) and the chemokines, monocyte chemoattractant protein (Mcp-1), macrophage inflammatory protein-2 (Mip-2) and keratinocyte derived chemokine (Kc) in the lung tissue at different time points after exposure. Results: Tnf mRNA expression levels increased late after DEP-inhalation, whereas the expression levels of Il-6, Mcp-1 and Kc increased early. The expression of Mip-2 was independent of TNF if the dose was above a certain level. The expression levels of the cytokines Kc, Mcp-1 and Il-6, were increased in the absence of TNF. Conclusion: Our data demonstrate that Tnf is not important in early DEP induced inflammation and rather exerts negative influence on Mcp-1 and Kc mRNA levels. This suggests that other signalling pathways are important, a candidate being one involving Mcp-1.

Original languageEnglish
Article number4
JournalParticle and Fibre Toxicology
Volume3
ISSN1743-8977
DOIs
StatePublished - 20 Feb 2006
Externally publishedYes
CitationsWeb of Science® Times Cited: No match on DOI
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