alexa Removal of Organic Content from Diesel Exhaust Particles Alters Cellular Responses of Primary Human Bronchial Epithelial Cells Cultured at an Air-Liquid Interface | Abstract
ISSN: 2161-0525

Journal of Environmental & Analytical Toxicology
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Research Article

Removal of Organic Content from Diesel Exhaust Particles Alters Cellular Responses of Primary Human Bronchial Epithelial Cells Cultured at an Air-Liquid Interface

Annalicia Vaughan1*, Svetlana Stevanovic2, Leanne E Morrison1, Ali Mohammad Pourkhesalian2, Mostafizur Rahman2, Ali Zare2, Branka Miljevic2, Felicia Goh1, Vandana Relan1, Rayleen V Bowman1, Kwun M Fong1, Steven E Bottle2, Zoran D Ristovski2 and Ian A Yang1
1The University of Queensland Thoracic Research Centre, The Prince Charles Hospital, Brisbane, Australia
2International Laboratory for Air Quality and Health, The Queensland University of Technology, Brisbane, Australia
Corresponding Author : Annalicia Vaughan
UQ Thoracic Research Centre
The Prince Charles Hospital
Rode Rd, Chermside, 4032 Queensland, Australia
Tel:
61731394110
E-mail: [email protected]
Received July 29, 2015; Accepted August 18, 2015; Published August 24, 2015
Citation: Vaughan A, Stevanovic S, Morrison LE, Pourkhesalian AM, Rahman M, et al. (2015) Removal of Organic Content from Diesel Exhaust Particles Alters Cellular Responses of Primary Human Bronchial Epithelial Cells Cultured at an Air- Liquid Interface. J Environ Anal Toxicol 5:316. doi:10.4172/2161-0525.1000316
Copyright: © 2015 Vaughan A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Background: Exposure to air pollutants, including diesel particulate matter, has been linked to adverse respiratory health effects. Inhaled diesel particulate matter contains adsorbed organic compounds. It is not clear whether the adsorbed organics or the residual components are more deleterious to airway cells. Using a physiologically relevant model, we investigated the role of diesel organic content on mediating cellular responses of primary human bronchial epithelial cells (HBECs) cultured at an air-liquid interface (ALI). Methods: Primary HBECs were cultured and differentiated at ALI for at least 28 days. To determine which component is most harmful, we compared primary HBEC responses elicited by residual (with organics removed) diesel emissions (DE) to those elicited by neat (unmodified) DE for 30 and 60 minutes at ALI, with cigarette smoke condensate (CSC) as the positive control, and filtered air as negative control. Cell viability (WST-1 cell proliferation assay), inflammation (TNF-α, IL-6 and IL-8 ELISA) and changes in gene expression (qRT-PCR for HO-1, CYP1A1, TNF-α and IL-8 mRNA) were measured. Results: Immunofluorescence and cytological staining confirmed the mucociliary phenotype of primary HBECs differentiated at ALI. Neat DE caused a comparable reduction in cell viability at 30 or 60 min exposures, whereas residual DE caused a greater reduction at 60 min. When corrected for cell viability, cytokine protein secretion for TNF-α, IL-6 and IL-8 were maximal with residual DE at 60 min. mRNA expression for HO-1, CYP1A1, TNF-α and IL-8 was not significantly different between exposures. Conclusion: This study provides new insights into epithelial cell responses to diesel emissions using a physiologically relevant aerosol exposure model. Both the organic content and residual components of diesel emissions play an important role in determining bronchial epithelial cell response in vitro. Future studies should be directed at testing potentially useful interventions against the adverse health effects of air pollution exposure.

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