title: Fine particulate matter from urban ambient and wildfire sources from California's San Joaquin Valley initiate differential inflammatory, oxidative stress, and xenobiotic responses in human bronchial epithelial cells.
abstract: Environmental particulate matter (PM) exposure has been correlated with pathogenesis of acute airway inflammatory disease such as asthma and COPD. PM size and concentration have been studied extensively, but the additional effects of particulate components such as biological material, transition metals, and polycyclic aromatic hydrocarbons could also impact initial disease pathogenesis. In this study, we compared urban ambient particulate matter (APM) collected from Fresno, California with wildfire (WF) particulate matter collected from Escalon, California on early transcriptional responses in human bronchial epithelial cells (HBE). Global gene expression profiling of APM treated HBE activated genes related to xenobiotic metabolism (CYP 1B1), endogenous ROS generation and response genes (DUOX1, SOD2, PTGS2) and pro-inflammatory responses associated with asthma or COPD such as IL-1α, IL-1β, IL-8, and CCL20. WF PM treatments also induced a pro-inflammatory gene response, but elicited a more robust xenobiotic metabolism and oxidative stress response. Inhibitor studies targeting endotoxin, ROS, and trace metals, found endotoxin inhibition had modest selective inhibition of inflammation while inhibition of hydrogen peroxide and transition metals had broad effects suggesting additional interactions with xenobiotic metabolism pathways. APM induced a greater inflammatory response while WF PM had more marked metabolism and ROS related responses.
authors.affiliation: School of Veterinary Medicine, Department of Pathology, Microbiology, and Immunology, University of California, Davis, CA 95616, United States.
authors.forename: L S
authors.initials: LS
authors.lastname: Nakayama Wong
authors.forename: H H
authors.initials: HH
authors.lastname: Aung
authors.forename: M W
authors.initials: MW
authors.lastname: Lamé
authors.forename: T C
authors.initials: TC
authors.lastname: Wegesser
authors.forename: D W
authors.initials: DW
authors.lastname: Wilson
mesh_terms: D000328:Adult; D000393:Air Pollutants / Q000633:toxicity*; D001980:Bronchi / Q000166:cytology; D002140:California; D002478:Cells, Cultured; D002947:Cities; D016207:Cytokines / Q000235:genetics; D004731:Endotoxins / Q000633:toxicity; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism; D005260:Female; D005390:Fires; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000187:drug effects*; D006801:Humans; D007249:Inflammation / Q000235:genetics; D020411:Oligonucleotide Array Sequence Analysis; D018384:Oxidative Stress / Q000235:genetics; D052638:Particulate Matter / Q000633:toxicity*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015262:Xenobiotics / Q000633:toxicity
chemical_list: D000393:Air Pollutants; D016207:Cytokines; D004731:Endotoxins; D052638:Particulate Matter; D015262:Xenobiotics