In vivo nasal challenge with diesel exhaust particles enhances expression of the CC chemokines rantes, MIP-1alpha, and MCP-3 in humans

Clin Immunol. 2000 Nov;97(2):140-5. doi: 10.1006/clim.2000.4921.

Abstract

Diesel exhaust particles (DEP) enhance allergic inflammation by increasing in vivo IgE and cytokine production in the human upper respiratory mucosa. CC chemokines have been shown to play an important role in inflammation. We examined whether DEP could alter the production of CC chemokines by cells residing in the human nasal mucosa. At both 6 and 24 h following intranasal DEP challenge, the levels of nasal RANTES, MIP-1alpha, and MCP-3 were significantly elevated compared to baseline. In contrast, DEP did not enhance levels of Eotaxin at any time, demonstrating that the action of DEP was not simply a global effect on all CC chemokines. Challenge with saline resulted in no significant change in expression of any chemokine at any time. Challenge with DEP also resulted in an increase in total cell counts in nasal lavage fluids. Increases in lymphocyte, monocyte/macrophage, and neutrophil cells were observed but there was no change in eosinophil cell numbers. In contrast, there was a significant enhancement of ECP protein levels in washes performed 6 to 24 h after DEP challenge. Elevated specific nasal chemokine expression following exposure to DEP likely participates in the inflammation, cellular infiltration, and increase in IgE observed in the absence of allergen.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Chemokine CCL3
  • Chemokine CCL4
  • Chemokine CCL5 / biosynthesis*
  • Chemokine CCL7
  • Chemokines, CC / biosynthesis*
  • Cytokines*
  • Female
  • Gene Expression
  • Humans
  • Macrophage Inflammatory Proteins / biosynthesis*
  • Macrophage Inflammatory Proteins / genetics
  • Male
  • Monocyte Chemoattractant Proteins / biosynthesis*
  • Monocyte Chemoattractant Proteins / genetics
  • Nasal Mucosa / metabolism*
  • RNA, Messenger / metabolism
  • Time Factors
  • Vehicle Emissions*

Substances

  • CCL7 protein, human
  • Chemokine CCL3
  • Chemokine CCL4
  • Chemokine CCL5
  • Chemokine CCL7
  • Chemokines, CC
  • Cytokines
  • Macrophage Inflammatory Proteins
  • Monocyte Chemoattractant Proteins
  • RNA, Messenger
  • Vehicle Emissions