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. 2017 Jul 18;51(14):8166-8175.
doi: 10.1021/acs.est.7b01967. Epub 2017 Jul 5.

Gene Expression Profiling in Human Lung Cells Exposed to Isoprene-Derived Secondary Organic Aerosol

Ying-Hsuan Lin  1 , Maiko Arashiro  1 , Phillip W Clapp  1 , Tianqu Cui  1 , Kenneth G Sexton  1 , William Vizuete  1 , Avram Gold  1 , Ilona Jaspers  1 , Rebecca C Fry  1 , Jason D Surratt  1
Affiliations

Gene Expression Profiling in Human Lung Cells Exposed to Isoprene-Derived Secondary Organic Aerosol

Ying-Hsuan Lin et al. Environ Sci Technol. .

Abstract

Secondary organic aerosol (SOA) derived from the photochemical oxidation of isoprene contributes a substantial mass fraction to atmospheric fine particulate matter (PM2.5). The formation of isoprene SOA is influenced largely by anthropogenic emissions through multiphase chemistry of its multigenerational oxidation products. Considering the abundance of isoprene SOA in the troposphere, understanding mechanisms of adverse health effects through inhalation exposure is critical to mitigating its potential impact on public health. In this study, we assessed the effects of isoprene SOA on gene expression in human airway epithelial cells (BEAS-2B) through an air-liquid interface exposure. Gene expression profiling of 84 oxidative stress and 249 inflammation-associated human genes was performed. Our results show that the expression levels of 29 genes were significantly altered upon isoprene SOA exposure under noncytotoxic conditions (p < 0.05), with the majority (22/29) of genes passing a false discovery rate threshold of 0.3. The most significantly affected genes belong to the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) transcription factor network. The Nrf2 function is confirmed through a reporter cell line. Together with detailed characterization of SOA constituents, this study reveals the impact of isoprene SOA exposure on lung responses and highlights the importance of further understanding its potential health outcomes.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Experimental profile of the photochemical oxidation experiment of isoprene. (A) Measurements of NO, NOx, O3 and aerosol mass concentration during the time course of experiment; (B) Decay of isoprene; (C) Shift of aerosol size distribution to greater values following the photochemical oxidation of isoprene, consistent with condensational SOA growth.
Figure 2
Figure 2
Chemical characterization of chamber-generated isoprene SOA: (A) GC/EI-MS total ion chromatogram (TIC) and (B) UPLC/(−)ESI-HR-QTOFMS extracted ion chromatograms (EICs) at m/z 198.99180, 215.02310, and 231.01801 corresponding to the MAE-, IEPOX-, and ISOPOOH-derived organosulfates, respectively.
Figure 3
Figure 3
Volcano plot of differentially expressed genes in BEAS-2B cells upon exposure to isoprene SOA. Dots in red indicate the significantly upregulated genes (23 genes). Dots in green indicate the significantly downregulated genes (6 genes). Dots in gray represent genes that did not significantly change in expression. A full list of differentially expressed genes can be found in Table 2.
Figure 4
Figure 4
Networks of gene-gene functional interactions for differentially expressed genes (FDR<0.3) derived from (A) NanoString human inflammation platform, and (B) human oxidative stress plus RT2 Profiler. Black nodes represent the input genes which were significantly altered upon isoprene SOA exposure, and gray nodes represent predicted related genes. Links denote associated pathways. The interactive gene network construction was performed and visualized using the GeneMANIA Cytoscape app.
Figure 5
Figure 5
Isoprene SOA constituents-induced Nrf2 activity in the reporter cell line. Data is presented as mean ± SD (N=3). Statistical analyses were done using a one-way ANOVA and Dunnett’s multiple comparisons post-hoc test. Significance represented as *p<0.05 and ****p<0.0001.
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