Abstract
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.
Highlights
Exposure to air pollution particulate matter (PM) is a potent generator of neuroinflammation in the central nervous system (CNS) [1, 2] and has been associated with decreased white matter volume and reduced cognition in older adults [3,4,5]
No differences existed in the medial corpus callosum for glial fibrillary acidic protein (GFAP) cell counts between filtered air (85.5 ± 13.2, n = 8) and nano-sized particulate matter (nPM) mice (85.6 ± 11.0, p = 0.98, n = 8) (Fig 1D and 1E)
Data from the present study demonstrates increased immunostaining of complement C5 protein, C5a receptor 1 (CD 88), and reactive microglia in the brain white matter of mice exposed to nPM
Summary
Exposure to air pollution particulate matter (PM) is a potent generator of neuroinflammation in the central nervous system (CNS) [1, 2] and has been associated with decreased white matter volume and reduced cognition in older adults [3,4,5]. Murine studies suggest that particulate matter exposure results in myelin loss in the CA1 stratum oriens of young mice, consistent with myelin reduction classically evident with aging [6]. While multiple CNS cell types are implicated in the inflammatory response, microglia have critical roles in particulate matterinduced CNS injury [7]. Microglial activation enables homeostatic phagocytosis and facilitates synaptic remodeling and brain maturation.
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