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

  • Saber, Anne T1
  • Jacobsen, Nicklas R1
  • Bornholdt, Jette1
  • Kjær, Sanna L1
  • Dybdahl, Marianne1
  • Risom, Lotte2
  • Loft, Steffen2
  • Vogel, Ulla1
  • Wallin, Håkan1
  • 1 National Institute of Occupational Health, Lersø Parkallé 105, Copenhagen, 2100, Denmark , Copenhagen
  • 2 Institute of Public Health, Copenhagen University, Øster Farimagsgade 5, opg. B, 2.sal, Copenhagen K, 1014, Denmark , Copenhagen K
Published Article
Particle and Fibre Toxicology
BioMed Central
Publication Date
Feb 20, 2006
DOI: 10.1186/1743-8977-3-4
Springer Nature


BackgroundParticulate 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.ResultsTnf 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.ConclusionOur 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.

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