Selective ATP-Binding Cassette Subfamily C Gene Expression and Proinflammatory Mediators Released by BEAS-2B after PM2.5, Budesonide, and Cotreated Exposures

Author:

Encarnación-Medina Jarline12,Rodríguez-Cotto Rosa I.234,Bloom-Oquendo Joseph1,Ortiz-Martínez Mario G.234,Duconge Jorge1,Jiménez-Vélez Braulio23ORCID

Affiliation:

1. School of Pharmacy, University of Puerto Rico, Medical Science Campus, San Juan, PR, USA

2. Center for Environmental and Toxicological Research, San Juan, PR, USA

3. School of Medicine, University of Puerto Rico, San Juan, PR, USA

4. Institute of Biomedical and Forensic Sciences Research of Puerto Rico Inc. (IBFSR), San Juan, PR, USA

Abstract

ATP-binding cassette subfamily C (ABCC) genes code for phase III metabolism proteins that translocate xenobiotic (e.g., particulate matter 2.5 (PM2.5)) and drug metabolites outside the cells. IL-6 secretion is related with the activation of the ABCC transporters. This study assesses ABCC1–4 gene expression changes and proinflammatory cytokine (IL-6, IL-8) release in human bronchial epithelial cells (BEAS-2B) exposed to PM2.5 organic extract, budesonide (BUD, used to control inflammation in asthmatic patients), and a cotreatment (Co-T: PM2.5 and BUD). A real-time PCR assay shows that ABCC1 was upregulated in BEAS-2B exposed after 6 and 7 hr to PM2.5 extract or BUD but downregulated after 6 hr of the Co-T. ABCC3 was downregulated after 6 hr of BUD and upregulated after 6 hr of the Co-T exposures. ABCC4 was upregulated after 5 hr of PM2.5 extract, BUD, and the Co-T exposures. The cytokine assay revealed an increase in IL-6 release by BEAS-2B exposed after 5 hr to PM2.5 extract, BUD, and the Co-T. At 7 hr, the Co-T decreases IL-6 release and IL-8 at 6 hr. In conclusion, the cotreatment showed an opposite effect on exposed BEAS-2B as compared with BUD. The results suggest an interference of the BUD therapeutic potential by PM2.5.

Funder

National Institutes of Health

Publisher

Hindawi Limited

Subject

Cell Biology,Immunology

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