News — The detrimental impact of air pollution on the outlook of ischemic stroke, which is triggered by reduced blood flow to the brain, has been demonstrated, yet the precise mechanism remains unclear. A group of scientists recently undertook a survey to establish if amplified brain inflammation, referred to as neuroinflammation, is the primary cause.
Following one week of intranasal exposure to urban aerosols from Beijing, China, mice exhibited elevated neuroinflammation and deteriorating motor function after ischemic stroke, in contrast to control mice that did not receive air pollution. Furthermore, this outcome was absent in mice treated with urban aerosols who lacked a receptor for polycyclic aromatic hydrocarbons (PAHs), chemicals released by the combustion of wood, garbage, fossil fuels, and tobacco. This implies that PAHs are implicated in both air pollution-related neuroinflammation and the heightened movement disorder linked with ischemic stroke.
"Our objective in conducting this research was to investigate the impact of air pollution on central nervous system disorders," stated Yasuhiro Ishihara, the senior author of the study and a professor in the Graduate School of Integrated Sciences for Life at Hiroshima University. "Specifically, we aimed to establish whether air pollution has any effect on the prognosis of ischemic stroke," added Ishihara.
The team took their investigation a step further by pinpointing particular constituents of air pollution that might directly contribute to decreased prognoses in ischemic stroke.
Their research uncovered evidence that intranasal exposure to air pollution from Beijing, China, led to elevated neuroinflammation in mice after ischemic stroke, achieved through the activation of microglial cells - immune cells located in the brain. Moreover, movement disorder was adversely impacted in ischemic stroke mice exposed to the same air pollution. In a second series of experiments, where Beijing air pollution was replaced with PM2.5 (tiny, aerosolized particles of air pollution that measure 2.5 microns or less in width) from Yokohama, Japan, comparable results were observed. This indicates that the PM2.5 fraction of urban air pollution comprises the chemical agent accountable for the increased neuroinflammation and reduced prognosis associated with ischemic stroke.
To pinpoint the chemicals in air pollution responsible for the reduced prognosis in ischemic stroke, the research team utilized mice lacking the aryl hydrocarbon receptor, a receptor that is stimulated by the existence of PAHs, to determine if exposure to Beijing air pollution would have a similar effect on mice without functional aryl hydrocarbon receptors. Mice without the aryl hydrocarbon receptor exhibited lower activation of microglial cells and movement disorder compared to normal mice, implying that the PAHs present in Beijing air pollution are responsible for at least some of the neuroinflammation and reduced prognosis observed in ischemic stroke mice exposed to air pollution.
The research team's ultimate objective is to gain a better understanding of the mechanism by which PM2.5 induces neuroinflammation since air pollution is initially inhaled into the respiratory tract. "Can small particles migrate from the nose to the brain? Does inflammation in the lungs or the body as a whole impact the brain's immune system?" Ishihara questioned.
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Other contributors include Nami Ishihara and Ami Oguro from the Program for Biomedical Science in the Graduate School of Integrated Sciences for Life at Hiroshima University in Higashi-Hiroshima, Japan; Miki Tanaka from Program for Biomedical Science in the Graduate School of Integrated Sciences for Life at Hiroshima University and the Laboratory for Pharmacotherapy and Experimental Neurology in the Kagawa School of Pharmaceutical Sciences at Tokushima Bunri University in Sanuki, Japan; Kouichi Itoh from the Laboratory for Pharmacotherapy and Experimental Neurology in the Kagawa School of Pharmaceutical Sciences at Tokushima Bunri University; Tomoaki Okuda from the Faculty of Science and Technology at Keio University in Yokohama, Japan; Yoshiaki Fujii-Kuriyama from the Medical Research Institute in Molecular Epidemiology at the Tokyo Medical and Dental University in Tokyo, Japan; Yu Nabetani from the Department of Applied Chemistry in the Faculty of Engineering at the University of Miyazaki in Miyazaki, Japan; Megumi Yamamoto from the Department of Environment and Public Health at the National Institute of Minamata Disease in Minamata, Japan; Christoph F. A. Vogel from the Department of Environmental Toxicology and the Center for Health and the Environment at the University of California Davis in Davis, California.
This work was supported by Research Fellowships for Young Scientists (Grant Number 20J10103), KAKENHI Grants from the Japan Society for the Promotion of Science (Grant Numbers 21K06702, 20H04341, 17H04714, 15KK0024), the Environmental Research and Technology Development Funds of the Environmental Restoration and Conservation Agency of Japan (Grant Numbers JPMEERF20165051 and JPMEERF20205007) and the National Institute of Environmental Health Sciences (Grant Numbers R01ES029126 and R01ES032827).
About Hiroshima University
Since its foundation in 1949, Hiroshima University has striven to become one of the most prominent and comprehensive universities in Japan for the promotion and development of scholarship and education. Consisting of 12 schools for undergraduate level and 5 graduate schools, ranging from natural sciences to humanities and social sciences, the university has grown into one of the most distinguished comprehensive research universities in Japan. English website:
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