Changed gene expression in brains of mice exposed to traffic in a highway tunnel

Inhal Toxicol. 2012 Aug;24(10):676-86. doi: 10.3109/08958378.2012.714004.

Abstract

Context: Air pollution has been suggested to have an impact on the brain.

Objective: The objective was to assess the expression of inflammation-related genes in the brains of mice that had been exposed for 5 days to a well-characterized traffic-polluted environment, i.e. a highway tunnel.

Materials and methods: Twenty C57BL6 mice were randomly allocated to four groups of five animals. Two groups were placed in the tunnel for 5 days (mean PM 2.5, 55.1 μg/m³, mean elemental carbon, EC 13.9 μg/m³) in cages with or without filter, two control groups were housed outside the tunnel. Animals were assessed within 24 hours after the last exposure day. Lung injury and inflammation were assessed by bronchoalveolar lavage (BAL) and histology. Blood leukocytosis and coagulation parameters were determined in peripheral blood. The olfactory bulb and hippocampus were analyzed for changes in expression of inflammatory genes and brain-derived neurotrophic factor (BDNF).

Results and discussion: Although carbon particles were abundant in alveolar macrophages of exposed mice and absent in non-exposed mice, there was no evidence of pulmonary or systemic inflammation. There was an increased expression of genes involved in inflammatory response (COX2, NOS2, NOS3, and NFE2L2) in the hippocampus of the exposed mice. In the olfactory bulb, a downregulation was found for IL1α, COX2, NFE2L2, IL6, and BDNF.

Conclusion: Although this short-term exposure to traffic-related pollution did not induce pulmonary or systemic inflammation, the expression of inflammatory genes was affected in different brain areas. The decreased BDNF expression in the olfactory bulb suggests lower brain neurotrophic support in response to traffic-related air pollution.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Air Pollutants / pharmacokinetics
  • Air Pollutants / toxicity*
  • Animals
  • Belgium
  • Brain-Derived Neurotrophic Factor / genetics
  • Brain-Derived Neurotrophic Factor / metabolism
  • Gene Expression Regulation / drug effects*
  • Hippocampus / drug effects*
  • Hippocampus / immunology
  • Hippocampus / metabolism
  • Inhalation Exposure / adverse effects*
  • Lung / drug effects
  • Lung / immunology
  • Lung / metabolism
  • Lung / pathology
  • Macrophages, Alveolar / drug effects
  • Macrophages, Alveolar / immunology
  • Macrophages, Alveolar / metabolism
  • Macrophages, Alveolar / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • NF-E2-Related Factor 2 / genetics
  • NF-E2-Related Factor 2 / metabolism
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism*
  • Neurons / drug effects
  • Neurons / immunology
  • Neurons / metabolism
  • Olfactory Bulb / drug effects*
  • Olfactory Bulb / immunology
  • Olfactory Bulb / metabolism
  • Organ Specificity
  • RNA, Messenger / metabolism
  • Random Allocation
  • Tissue Distribution
  • Urban Health
  • Vehicle Emissions / analysis
  • Vehicle Emissions / toxicity*

Substances

  • Air Pollutants
  • Brain-Derived Neurotrophic Factor
  • NF-E2-Related Factor 2
  • Nerve Tissue Proteins
  • Nfe2l2 protein, mouse
  • RNA, Messenger
  • Vehicle Emissions