Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Leonard Davis School of Gerontology, University of Southern California, Los Angeles, California, United States of America.
PLoS One. 2018 Nov 5;13(11):e0206934. doi: 10.1371/journal.pone.0206934. eCollection 2018.
Epidemiological studies have established an association between air pollution particulate matter exposure (PM2.5) and neurocognitive decline. Experimental data suggest that microglia play an essential role in air pollution PM-induced neuroinflammation and oxidative stress. This study examined the effect of nano-sized particulate matter (nPM) on complement C5 deposition and microglial activation in the corpus callosum of mice (C57BL/6J males). nPM was collected in an urban Los Angeles region impacted by traffic emissions. Mice were exposed to 10 weeks of re-aerosolized nPM or filtered air for a cumulative 150 hours. nPM-exposed mice exhibited reactive microglia and 2-fold increased local deposition of complement C5/ C5α proteins and complement component C5a receptor 1 (CD88) in the corpus callosum. However, serum C5 levels did not differ between nPM and filtered air cohorts. These findings demonstrate white matter C5 deposition and microglial activation secondary to nPM exposure. The C5 upregulation appears to be localized to the brain.
流行病学研究已经证实,空气污染细颗粒物(PM2.5)暴露与神经认知能力下降之间存在关联。实验数据表明,小胶质细胞在空气污染 PM 引起的神经炎症和氧化应激中发挥着重要作用。本研究探讨了纳米级颗粒物(nPM)对小鼠(C57BL/6J 雄性)胼胝体中补体 C5 沉积和小胶质细胞激活的影响。nPM 是在受交通排放影响的洛杉矶市区收集的。小鼠暴露于再气溶胶化的 nPM 或过滤空气中 10 周,累计暴露 150 小时。暴露于 nPM 的小鼠表现出反应性小胶质细胞,以及在胼胝体中补体 C5/C5α 蛋白和补体成分 C5a 受体 1(CD88)的局部沉积增加了两倍。然而,nPM 和过滤空气组之间的血清 C5 水平没有差异。这些发现表明,由于 nPM 暴露导致了白质 C5 的沉积和小胶质细胞的激活。C5 的上调似乎局限于大脑。