Use of human bronchial epithelial cells (BEAS-2B) to study immunological markers resulting from exposure to PM(2.5) organic extract from Puerto Rico.
Fine particulate air pollutants, mainly their organic fraction, have been demonstrated to be associated with cardiovascular and respiratory health problems. Puerto Rico has been reported to have the highest prevalence of pulmonary diseases (e.g., asthma) in the United States. The aim of this study was to assess, for the first time, the immunological response of human bronchial epithelial cells (BEAS-2B) to organic extracts isolated from airborne particulate matter (PM(2.5)) in Puerto Rico. Organic extracts from PM(2.5) collected throughout an 8-month period (2000-2001) were pooled (composite) in order to perform chemical analysis and biological activity testing. BEAS-2B cells were exposed to PM(2.5) organic extract to assess cytotoxicity, levels of cytokines and relative gene expression of MHC-II, hPXR and CYP3A5. Our findings show that organic PM(2.5) consist of toxic as well as bioactive components that can regulate the secretion of cytokines in BEAS-2B, which could modulate inflammatory response in the lung. Trace element analyses confirmed the presence of metals in organic extracts highlighting the relative high abundance of Cu and Zn in polar organic extracts. Polar organic extracts exhibited dose-dependant toxicity and were found to significantly induce the release of interleukin 6 (IL-6), IL-1beta and IL-7 while significantly inhibiting the secretion of IL-8, G-CSF and MCP-1. Moreover, MHC-II transcriptional activity was up-regulated after 24 h of exposure, whereas PXR and CYP3A5 were down-regulated. This research provides a new insight into the effects of PM(2.5) organic fractions on specific effectors and their possible role in the development of respiratory inflammatory diseases in Puerto Rico.
Fuentes-Mattei
Enrique
E
Department of Biochemistry, School of Medicine, Medical Sciences Campus, University of Puerto Rico, San Juan, Puerto Rico.
Rivera
Evasomary
E
Gioda
Adriana
A
Sanchez-Rivera
Diana
D
Roman-Velazquez
Felix R
FR
Jimenez-Velez
Braulio D
BD
D000395:Air Pollutants, Occupational / Q000032:analysis / Q000633:toxicity*; D015415:Biomarkers / Q000032:analysis*; D001980:Bronchi / Q000166:cytology / Q000276:immunology / Q000473:pathology*; D002460:Cell Line; D051544:Cytochrome P-450 CYP3A / Q000096:biosynthesis; D016207:Cytokines / Q000032:analysis; D004784:Environmental Monitoring; D004847:Epithelial Cells / Q000276:immunology* / Q000473:pathology*; D005802:Genes, MHC Class II / Q000187:drug effects; D015802:HLA-DR2 Antigen / Q000096:biosynthesis; D006801:Humans; D052638:Particulate Matter / Q000032:analysis / Q000633:toxicity*; D000077297:Pregnane X Receptor; D011647:Puerto Rico; D012333:RNA, Messenger / Q000096:biosynthesis / Q000302:isolation & purification; D011987:Receptors, Steroid / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013489:Suppression, Genetic / Q000187:drug effects; D014131:Trace Elements / Q000633:toxicity; D015533:Transcriptional Activation
D000395:Air Pollutants, Occupational; D015415:Biomarkers; D016207:Cytokines; D015802:HLA-DR2 Antigen; D052638:Particulate Matter; D000077297:Pregnane X Receptor; D012333:RNA, Messenger; D011987:Receptors, Steroid; D014131:Trace Elements; C510164:CYP3A5 protein, human; D051544:Cytochrome P-450 CYP3A