ArticleToxicological sciences : an official journal of the Society of Toxicology2018
Aging Exacerbates Neuroinflammatory Outcomes Induced by Acute Ozone Exposure.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 59 citations in OpenAlex.
- A New Mouse Model for Ozone Health Effects Research.Environmental health perspectives · 2026Article
- Sex dimorphism in the cardiovascular responses to d-galactose-induced accelerated aging: effects of HO-1 modulation.GeroScience · 2026Article
- Neurometabolomic impacts of wood smoke and protective benefits of anti-aging therapeutics in aged female C57BL/6J mice.Particle and fibre toxicology · 2025Article
- Unraveling the Complex Interplay Between Neuroinflammation and Depression: A Comprehensive Review.International journal of molecular sciences · 2025Review
- What is the relationship between exposure to environmental pollutants and severe mental disorders? A systematic review on shared biological pathways.Brain, behavior, & immunity - health · 2025Review
- Article
- Exposure to multiple ambient air pollutants changes white matter microstructure during early adolescence with sex-specific differences.Communications medicine · 2024Article
- Multi-omics analysis reveals the dynamic interplay between Vero host chromatin structure and function during vaccinia virus infection.Communications biology · 2024Article
- Association of Gaseous Ambient Air Pollution and Dementia-Related Neuroimaging Markers in the ARIC Cohort, Comparing Exposure Estimation Methods and Confounding by Study Site.Environmental health perspectives · 2024Article
- Peripheral HMGB1 is linked to OAlzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Application of mesenchymal stem cells for anti-senescence and clinical challenges.Stem cell research & therapy · 2023Review
- Biomass smoke inhalation promotes neuroinflammatory and metabolomic temporal changes in the hippocampus of female mice.Journal of neuroinflammation · 2023Article
- Neuroinflammatory and Metabolomic Temporal Dynamics Following Wood Smoke Inhalation.Research square · 2023Article
- Acute Ozone-Induced Transcriptional Changes in Markers of Oxidative Stress and Glucocorticoid Signaling in the Rat Hippocampus and Hypothalamus Are Sex-Specific.International journal of molecular sciences · 2023Article
- The bidirectional lung brain-axis of amyloid-β pathology: ozone dysregulates the peri-plaque microenvironment.Brain : a journal of neurology · 2023Article
- Effects of Ozone on Sickness and Depressive-like Behavioral and Biochemical Phenotypes and Their Regulation by Serum Amyloid A in Mice.International journal of molecular sciences · 2023Article
- Current practice and recommendations for advancing how human variability and susceptibility are considered in chemical risk assessment.Environmental health : a global access science source · 2023Review
- Aging, longevity, and the role of environmental stressors: a focus on wildfire smoke and air quality.Frontiers in toxicology · 2023Review
- Air Pollution: Possible Interaction between the Immune and Nervous System?International journal of environmental research and public health · 2022Review
- Association between air pollution and CSF sTREM2 in cognitively normal older adults: The CABLE study.Annals of clinical and translational neurology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
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 (O3) exposure in aged mice, where increased blood-brain barrier (BBB) permeability may confer vulnerability to neuroinflammatory outcomes. C57BL/6 male mice, aged 8-10 weeks or 12-18 months were exposed to either filtered air or 1.0 ppm O3 for 4 h; animals received a single IP injection of sodium fluorescein (FSCN) 20 h postexposure. One-hour post-FSCN injection, animals were transcardially perfused for immunohistochemical analysis of BBB permeability. β-amyloid protein expression was assessed via ELISA. Flow cytometric characterization of infiltrating immune cells, including neutrophils, macrophages, and microglia populations was performed 20 h post-O3 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 O3 exposure. Cortical and limbic regions in aged brains had increased reactive microgliosis and β-amyloid protein expression after O3 insult. The aged cerebellum was particularly vulnerable to acute O3 exposure with increased populations of infiltrating neutrophils, peripheral macrophages/monocytes, and Ly6C+ inflammatory monocytes after insult, which were not significantly increased in the young cerebellum. O3 exposure increased the penetration of FSCN beyond the BBB, the infiltration of peripheral immune cells, and reactive gliosis of microglia. Thus, the aged BBB is vulnerable to insult and becomes highly penetrable in response to O3 exposure, leading to greater neuroinflammatory outcomes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.