Dataset Information

Oxidative stress and aromatic hydrocarbon response of human bronchial epithelial cells exposed to petro- or biodiesel exhaust treated with a diesel particulate filter.

ABSTRACT: The composition of diesel exhaust has changed over the past decade due to the increased use of alternative fuels, like biodiesel, and to new regulations on diesel engine emissions. Given the changing nature of diesel fuels and diesel exhaust emissions, a need exists to understand the human health implications of switching to "cleaner" diesel engines run with particulate filters and engines run on alternative fuels like biodiesel. We exposed well-differentiated normal human bronchial epithelial cells to fresh, complete exhaust from a diesel engine run (1) with and without a diesel particulate filter and (2) using either traditional petro- or alternative biodiesel. Despite the lowered emissions in filter-treated exhaust (a 91-96% reduction in mass), significant increases in transcripts associated with oxidative stress and polycyclic aromatic hydrocarbon response were observed in all exposure groups and were not significantly different between exposure groups. Our results suggest that biodiesel and filter-treated diesel exhaust elicits as great, or greater a cellular response as unfiltered, traditional petrodiesel exhaust in a representative model of the bronchial epithelium.

SUBMITTER: Hawley B

PROVIDER: S-EPMC4833025 | biostudies-literature | 2014 Oct

REPOSITORIES: biostudies-literature

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Oxidative stress and aromatic hydrocarbon response of human bronchial epithelial cells exposed to petro- or biodiesel exhaust treated with a diesel particulate filter.

Hawley Brie B L'Orange Christian C Olsen Dan B DB Marchese Anthony J AJ Volckens John J

Toxicological sciences : an official journal of the Society of Toxicology 20140724 2

The composition of diesel exhaust has changed over the past decade due to the increased use of alternative fuels, like biodiesel, and to new regulations on diesel engine emissions. Given the changing nature of diesel fuels and diesel exhaust emissions, a need exists to understand the human health implications of switching to "cleaner" diesel engines run with particulate filters and engines run on alternative fuels like biodiesel. We exposed well-differentiated normal human bronchial epithelial c ...[more]

PMID: 25061111

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Project description:BackgroundDiesel exhaust particles (DEP) are a major component of outdoor air pollution. DEP mediated pulmonary effects are plausibly linked to inflammatory and oxidative stress response in which macrophages (MQ), epithelial cells and their cell-cell interaction plays a crucial role. Therefore, in this study we aimed at studying the cellular crosstalk between airway epithelial cells with MQ and MQ polarization following exposure to aerosolized DEP by assessing inflammation, oxidative stress, and MQ polarization response markers.MethodLung mucosa models including primary bronchial epithelial cells (PBEC) cultured at air-liquid interface (ALI) were co-cultured without (PBEC-ALI) and with MQ (PBEC-ALI/MQ). Cells were exposed to 12.7 μg/cm2 aerosolized DEP using XposeALI®. Control (sham) models were exposed to clean air. Cell viability was assessed. CXCL8 and IL-6 were measured in the basal medium by ELISA. The mRNA expression of inflammatory markers (CXCL8, IL6, TNFα), oxidative stress (NFKB, HMOX1, GPx) and MQ polarization markers (IL10, IL4, IL13, MRC1, MRC2 RETNLA, IL12 andIL23) were measured by qRT-PCR. The surface/mRNA expression of TLR2/TLR4 was detected by FACS and qRT-PCR.ResultsIn PBEC-ALI exposure to DEP significantly increased the secretion of CXCL8, mRNA expression of inflammatory markers (CXCL8, TNFα) and oxidative stress markers (NFKB, HMOX1, GPx). However, mRNA expressions of these markers (CXCL8, IL6, NFKB, and HMOX1) were reduced in PBEC-ALI/MQ models after DEP exposure. TLR2 and TLR4 mRNA expression increased after DEP exposure in PBEC-ALI. The surface expression of TLR2 and TLR4 on PBEC was significantly reduced in sham-exposed PBEC-ALI/MQ compared to PBEC-ALI. After DEP exposure surface expression of TLR2 was increased on PBEC of PBEC-ALI/MQ, while TLR4 was decreased in both models. DEP exposure resulted in similar expression pattern of TLR2/TLR4 on MQ as in PBEC. In PBEC-ALI/MQ, DEP exposure increased the mRNA expression of anti-inflammatory M2 macrophage markers (IL10, IL4, IL13, MRC1, MRC2).ConclusionThe cellular interaction of PBEC with MQ in response to DEP plays a pivotal role for MQ phenotypic alteration towards M2-subtypes, thereby promoting an efficient resolution of the inflammation. Furthermore, this study highlighted the fact that cell-cell interaction using multicellular ALI-models combined with an in vivo-like inhalation exposure system is critical in better mimicking the airway physiology compared with traditional cell culture systems.

Project description:The carcinogenic effects of individual polycyclic aromatic hydrocarbons (PAH) are well established. However, their potency within an environmental complex mixture is uncertain. We evaluated the influence of diesel exhaust particulate matter on PAH-induced cytochrome P450 (CYP) activity, PAH-DNA adduct formation, expression of certain candidate genes and the frequency of tumor initiation in the two-stage Sencar mouse model. To this end, we monitored the effects of treatment of mice with diesel exhaust, benzo[a]pyrene (BP), dibenzo[a,l]pyrene (DBP), or a combination of diesel exhaust with either carcinogenic PAH. The applied diesel particulate matter (SRM(1975)) altered the tumor initiating potency of DBP: a statistically significant decrease in overall tumor and carcinoma burden was observed following 25 weeks of promotion with 12-O-tetradecanoylphorbol-13-acetate (TPA), compared with DBP exposure alone. From those mice that were treated at the beginning of the observation period with 2 nmol DBP all survivors developed tumors (9 out of 9 animals, 100%). Among all tumors counted at the end, nine carcinomas were detected and an overall tumor incidence of 2.6 tumors per tumor-bearing animal (TBA) was determined. By contrast, co-treatment of DBP with 50mg SRM(1975) led to a tumor rate of only 66% (19 out of 29 animals), occurrence of only three carcinomas in 29 animals and an overall rate of 2.1 tumors per TBA (P=0.04). In contrast to the results with DBP, the tumor incidence induced by 200 nmol BP was found slightly increased when co-treatment with SRM(1975) occurred (71% vs. 85% after 25 weeks). Despite this difference in tumor incidence, the numbers of carcinomas and tumors per TBA did not differ statistically significant between both treatment groups possibly due to the small size of the BP treatment group. Since bioactivation of DBP, but not BP, predominantly depends on CYP1B1 enzyme activity, SRM(1975) affected PAH-induced carcinogenesis in an antagonistic manner when CYP1B1-mediated bioactivation was required. The explanation most likely lies in the much stronger inhibitory effects of certain PAHs present in diesel exhaust on CYP1B1 compared to CYP1A1. In the present study we also found molecular markers such as highly elevated AKR1C21 and TNFRSF21 gene expression levels in tumor tissue derived from animals co-treated with SRM(1975) plus DBP. Therefore we validate microarray data as a source to uncover transcriptional signatures that may provide insights into molecular pathways affected following exposure to environmental complex mixtures such as diesel exhaust particulates.

Dataset Information

Oxidative stress and aromatic hydrocarbon response of human bronchial epithelial cells exposed to petro- or biodiesel exhaust treated with a diesel particulate filter.

Publications

Oxidative stress and aromatic hydrocarbon response of human bronchial epithelial cells exposed to petro- or biodiesel exhaust treated with a diesel particulate filter.

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