Flemish Institute for Technological Research (VITO), Mol, Belgium.
Inhal Toxicol. 2012 Aug;24(10):676-86. doi: 10.3109/08958378.2012.714004.
Air pollution has been suggested to have an impact on the brain.
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.
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).
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.
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.
空气污染被认为对大脑有影响。
评估在经过 5 天暴露于经过充分描述的交通污染环境(即高速公路隧道)的情况下,小鼠大脑中与炎症相关的基因表达情况。
20 只 C57BL6 小鼠被随机分配到四个五动物组。两组在隧道中放置 5 天(平均 PM2.5 为 55.1μg/m³,平均元素碳 EC 为 13.9μg/m³),笼子中装有或不装有过滤器,两组对照组在隧道外饲养。在最后一次暴露后 24 小时内对动物进行评估。通过支气管肺泡灌洗(BAL)和组织学评估肺损伤和炎症。在外周血中测定白细胞增多和凝血参数。分析嗅球和海马中炎症基因和脑源性神经营养因子(BDNF)表达的变化。
尽管暴露于碳颗粒的肺泡巨噬细胞中存在大量碳颗粒,而未暴露于碳颗粒的巨噬细胞中不存在碳颗粒,但没有证据表明存在肺或全身炎症。暴露于污染的小鼠海马中与炎症反应相关的基因(COX2、NOS2、NOS3 和 NFE2L2)表达增加。在嗅球中,IL1α、COX2、NFE2L2、IL6 和 BDNF 的表达下调。
尽管这种短期接触交通相关污染不会引起肺或全身炎症,但不同脑区的炎症基因表达受到影响。嗅球中 BDNF 表达降低表明交通相关空气污染对大脑神经营养支持降低。