Aging Exacerbates Neuroinflammatory Outcomes Induced by Acute Ozone Exposure [electronic resource]

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Tác giả:

Ngôn ngữ: eng

Ký hiệu phân loại: 630.7 Education, research, related topics

Thông tin xuất bản: Bethesda, Md. : Oak Ridge, Tenn. : National Institutes of Health (U.S.) ; Distributed by the Office of Scientific and Technical Information, U.S. Dept. of Energy, 2018

Mô tả vật lý: Size: p. 123-139 : , digital, PDF file.

Bộ sưu tập: Metadata

ID: 260277

 The role of environmental stressors, particularly exposure to air pollution, in the development of neurodegenerative disease remains underappreciated. We examined the neurological effects of acute ozone (O<
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 ) exposure in aged mice, where increased blood brain barrier (BBB) permeability may confer vulnerability to neuroinflammatory outcomes. C<
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 BL/6 male mice, aged 8-10 weeks or 12?18 months were exposed to either filtered air (FA) or 1.0 ppm O<
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  for 4 hours
  animals received a single IP injection of sodium fluorescein (FSCN) 20 hours post-exposure. One-hour post-FSCN injection, animals were transcardially perfused for immunohistochemical analysis of BBB permeability. ?-amyloid protein expression was assessed via ELISA. Flow cytometric characterization of infiltrating immune cells, including neutrophils, macrophages, and microglia populations was performed 20 hours post-O<
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  exposure. Flow cytometry analysis of brains revealed increased microglia ?activation? and presentation of CD11b, F4/80 and MHCII in aged animals relative to younger ones
  these age-induced differences were potentiated by acute O<
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  exposure. Cortical and limbic regions in aged brains had increased reactive microgliosis and ?-amyloid protein expression after O<
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  insult. The aged cerebellum was particularly vulnerable to acute O<
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  exposure with increased populations of infiltrating neutrophils, peripheral macrophages/monocytes, and Ly6C<
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  inflammatory monocytes after insult, which were not significantly increased in the young cerebellum. O<
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  exposure increased the penetration of FSCN beyond the BBB, the infiltration of peripheral immune cells, and reactive gliosis of microglia. Furthermore, the aged BBB is vulnerable to insult and becomes highly penetrable in response to O<
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  exposure, leading to greater neuroinflammatory outcomes.
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