Biomedical Sciences ETDs
Publication Date
Spring 5-16-2026
Abstract
Wildfires in the United States have increased over the past 40 years due to climate change, with smoke exposure linked to cardiovascular, respiratory, and emerging neurological health effects. This work investigates the timeline and immune mechanisms of wildfire smoke–induced neuroinflammation and evaluates potential interventions, including the Rho kinase inhibitor fasudil, and the lipid mediator Resolvin D1 (RvD1). Female C57BL/6 mice were exposed to woodsmoke over 14 days, with neuroinflammatory outcomes assessed at 1, 14, and 28 days post-exposure. Results reveal time- and diet-dependent infiltration of peripheral immune cells, particularly CD4 T cells, alongside peak expression of adhesion molecules shortly after exposure. Saturated fat diets exacerbated and prolonged inflammation, while fasudil reduced immune cell infiltration, supporting a blood–brain barrier mechanism. RvD1 mitigated inflammation and accelerated resolution. These findings highlight systemic immune involvement in smoke-induced neuroinflammation and suggest therapeutic and dietary strategies for reducing risk.
Keywords
Toxicology, Neuroimmunology, Particulate Matter, Adaptive Immunity
Document Type
Dissertation
Language
English
Degree Name
Biomedical Sciences
Level of Degree
Doctoral
Department Name
Biomedical Sciences Graduate Program
First Committee Member (Chair)
Russell Morton
Second Committee Member
Matthew Campen
Third Committee Member
Sarah Blossom
Fourth Committee Member
Shahani Noor
Recommended Citation
Baird, Brenna. "Wildfire Smoke-Induced Neuroinflammation and Interventions to Prevent and Modulate Immune Cell Infiltration into the Brain." (2026). https://digitalrepository.unm.edu/biom_etds/319