Brain cytokine and chemokine mRNA expression in mice induced by intranasal instillation with ultrafine carbon black

Toxicol Lett. 2006 May 25;163(2):153-60. doi: 10.1016/j.toxlet.2005.10.006. Epub 2005 Nov 15.

Abstract

Ambient air ultrafine particles (UFPs) have gained enormous attention to many researchers with recent evidence showing them to have more hazardous effects on human health than larger ambient particles. Studies focusing the possibility of effects on brain are quite limited. To examine the effect of ultrafine carbon black (ufCB) on mice brain, we instilled 125 microg of 14 nm or 95 nm CB into the nostrils of 8-week-old male BALB/c mice, once a week for 4 weeks. Four hours after the last instillation, we collected olfactory bulb and hippocampus and detected the expression of cytokine and chemokine mRNA by quantitative real-time PCR method. In this study, we found the induction of proinflammatory cytokines (interleukin-1 beta and tumor necrosis factor-alpha and chemokines (monocyte chemoattractant protein-1/CCL2, macrophage inflammatory protein-1 alpha/CCL3), and monokine induced interferon-gamma/CXC chemokine ligand (CXCL9) mRNA in brain olfactory bulb, not in the hippocampus of mice instilled with 14 nm ufCB intranasally. We suggest that the intranasal instillation of ufCB may influence the brain immune function depending on their size. To our knowledge, this is the first study to demonstrate region-specific brain cytokine and chemokine mRNA-induction in mice triggered by intranasal instillation of specific-sized ufCB, in a physiologically relevant condition.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Intranasal
  • Animals
  • Carbon / toxicity*
  • Chemokine CCL2 / genetics
  • Chemokine CCL2 / metabolism
  • Chemokine CCL3
  • Chemokine CCL4
  • Chemokine CXCL9
  • Chemokines, CC / genetics
  • Chemokines, CC / metabolism
  • Chemokines, CXC / genetics
  • Chemokines, CXC / metabolism
  • Cytokines / genetics
  • Cytokines / metabolism*
  • Disease Models, Animal
  • Gene Expression / drug effects
  • Hippocampus / drug effects*
  • Hippocampus / metabolism
  • Hippocampus / pathology
  • Interleukin-1 / genetics
  • Interleukin-1 / metabolism
  • Macrophage Inflammatory Proteins / genetics
  • Macrophage Inflammatory Proteins / metabolism
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Olfactory Bulb / drug effects*
  • Olfactory Bulb / metabolism
  • Olfactory Bulb / pathology
  • Particle Size
  • RNA, Messenger / metabolism
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Ccl2 protein, mouse
  • Ccl3 protein, mouse
  • Chemokine CCL2
  • Chemokine CCL3
  • Chemokine CCL4
  • Chemokine CXCL9
  • Chemokines, CC
  • Chemokines, CXC
  • Cxcl9 protein, mouse
  • Cytokines
  • Interleukin-1
  • Macrophage Inflammatory Proteins
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Carbon