<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Scieszka D</submitter><funding>The National Institute of Environmental Health Sciences</funding><funding>NIA NIH HHS</funding><funding>NIEHS NIH HHS</funding><funding>NIMHD NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>149-162</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8883349</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>186(1)</volume><pubmed_abstract>Utilizing a mobile laboratory located >300 km away from wildfire smoke (WFS) sources, this study examined the systemic immune response profile, with a focus on neuroinflammatory and neurometabolomic consequences, resulting from inhalation exposure to naturally occurring wildfires in California, Arizona, and Washington in 2020. After a 20-day (4 h/day) exposure period in a mobile laboratory stationed in New Mexico, WFS-derived particulate matter (WFPM) inhalation resulted in significant neuroinflammation while immune activity in the peripheral (lung, bone marrow) appeared to be resolved in C57BL/6 mice. Importantly, WFPM exposure increased cerebrovascular endothelial cell activation and expression of adhesion molecules (VCAM-1 and ICAM-1) in addition to increased glial activation and periph</pubmed_abstract><journal>Toxicological sciences : an official journal of the Society of Toxicology</journal><pubmed_title>Neuroinflammatory and Neurometabolomic Consequences From Inhaled Wildfire Smoke-Derived Particulate Matter in the Western United States.</pubmed_title><pmcid>PMC8883349</pmcid><funding_grant_id>R01 AG070776</funding_grant_id><funding_grant_id>P50 MD015706</funding_grant_id><funding_grant_id>R01 ES026673</funding_grant_id><funding_grant_id>P42 ES025589</funding_grant_id><funding_grant_id>P20 GM130422</funding_grant_id><funding_grant_id>R01 ES014639</funding_grant_id><pubmed_authors>Canal CG</pubmed_authors><pubmed_authors>Hunter R</pubmed_authors><pubmed_authors>Begay J</pubmed_authors><pubmed_authors>Lin Y</pubmed_authors><pubmed_authors>Wagner J</pubmed_authors><pubmed_authors>Morishita M</pubmed_authors><pubmed_authors>Mostovenko E</pubmed_authors><pubmed_authors>Scieszka D</pubmed_authors><pubmed_authors>Klaver Z</pubmed_authors><pubmed_authors>Campen MJ</pubmed_authors><pubmed_authors>Gu H</pubmed_authors><pubmed_authors>Bolt A</pubmed_authors><pubmed_authors>Bleske B</pubmed_authors><pubmed_authors>Ottens AK</pubmed_authors><pubmed_authors>McVeigh C</pubmed_authors><pubmed_authors>Harkema JR</pubmed_authors><pubmed_authors>Herbert G</pubmed_authors><pubmed_authors>Noor S</pubmed_authors><pubmed_authors>Bitsui M</pubmed_authors><pubmed_authors>Lucas S</pubmed_authors><pubmed_authors>Galewsky J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Neuroinflammatory and Neurometabolomic Consequences From Inhaled Wildfire Smoke-Derived Particulate Matter in the Western United States.</name><description>Utilizing a mobile laboratory located >300 km away from wildfire smoke (WFS) sources, this study examined the systemic immune response profile, with a focus on neuroinflammatory and neurometabolomic consequences, resulting from inhalation exposure to naturally occurring wildfires in California, Arizona, and Washington in 2020. After a 20-day (4 h/day) exposure period in a mobile laboratory stationed in New Mexico, WFS-derived particulate matter (WFPM) inhalation resulted in significant neuroinflammation while immune activity in the peripheral (lung, bone marrow) appeared to be resolved in C57BL/6 mice. Importantly, WFPM exposure increased cerebrovascular endothelial cell activation and expression of adhesion molecules (VCAM-1 and ICAM-1) in addition to increased glial activation and periph</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Feb</publication><modification>2026-05-05T18:11:15.36Z</modification><creation>2025-04-06T13:59:09.897Z</creation></dates><accession>S-EPMC8883349</accession><cross_references><pubmed>34865172</pubmed><doi>10.1093/toxsci/kfab147</doi></cross_references></HashMap>