Developmental exposure to air pollution particulates increases asthma severity, alters the RNA transcriptome, and DNA methylation in female adult progeny [WGMS]
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ABSTRACT:
PROVIDER: PRJNA1202100 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31913319_1.fastq.gz | Fastqsanger.gz | |||
| SRR31913319_2.fastq.gz | Fastqsanger.gz | |||
| SRR31913320_1.fastq.gz | Fastqsanger.gz | |||
| SRR31913320_2.fastq.gz | Fastqsanger.gz | |||
| SRR31913321_1.fastq.gz | Fastqsanger.gz |
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Project description:Maternal exposure to particulate air pollution increases the incidence and severity of asthma in offspring, yet the mechanisms for this are unclear. Known susceptibility loci are a minor component of this effect. We interrogate a mouse allergic airway disease model to assess epigenetic associations between maternal air pollution exposure and asthma-like responses in offspring. Maternal air pollution exposure increased allergic airway disease severity in adult offspring associated with a suppressed transcriptomic response to allergen. Control progeny showed differential expression of 2842 genes across several important pathways, including the SMAD and TGFβR pathways, whilst air pollutant progeny showed an 80% reduction in differentially expressed genes and abrogation of many pathway associations. Whole genome CpG methylome analysis following allergen challenge detected differential methylation regions across the genome. Approximately 20% of differentially expressed genes were associated with differential methylation. Differentially methylated regions were markedly reduced in offspring of air pollution exposed mothers, and this was most evident in intronic regions and some transposable element classes. This study shows that allergic airways disease in adult offspring of PM2.5 exposed mothers had a markedly repressed transcriptomic response, a proportion of which was associated with identifiable changes in the lung’s methylome. The results point to an epigenetic contribution to the severity of asthma in offspring of mothers exposed to particulate air pollution.
2025-03-12 | GSE285243 | GEO
Project description:Maternal exposure to particulate air pollution increases the incidence and severity of asthma in offspring, yet the mechanisms for this are unclear. Known susceptibility loci are a minor component of this effect. We interrogate a mouse allergic airway disease model to assess epigenetic associations between maternal air pollution exposure and asthma-like responses in offspring. Maternal air pollution exposure increased allergic airway disease severity in adult offspring associated with a suppressed transcriptomic response to allergen. Control progeny showed differential expression of 2842 genes across several important pathways, including the SMAD and TGFβR pathways, whilst air pollutant progeny showed an 80% reduction in differentially expressed genes and abrogation of many pathway associations. Whole genome CpG methylome analysis following allergen challenge detected differential methylation regions across the genome. Approximately 20% of differentially expressed genes were associated with differential methylation. Differentially methylated regions were markedly reduced in offspring of air pollution exposed mothers, and this was most evident in intronic regions and some transposable element classes. This study shows that allergic airways disease in adult offspring of PM2.5 exposed mothers had a markedly repressed transcriptomic response, a proportion of which was associated with identifiable changes in the lung’s methylome. The results point to an epigenetic contribution to the severity of asthma in offspring of mothers exposed to particulate air pollution.
2025-03-12 | GSE285128 | GEO
Project description:Developmental exposure to air pollution particulates increases asthma severity, alters the RNA transcriptome, and DNA methylation in female adult progeny [RNA-Seq]
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Project description:Rationale: DNA methylation plays a critical role in asthma development, but differences in DNA methylation associated with asthma severity, especially among adults, are less well-defined. Changes in DNA methylation are influenced by exposure to air pollution, which is a risk factor for asthma exacerbation and severity. Here, we examined how DNA methylomic patterns in adult asthmatics differ by asthma severity and exposure to different components of air pollution. Methods: Peripheral blood CD3+ T cells from adult asthmatics in Beijing, China were serially collected from 37 patients (130 samples total) and analyzed for global DNA methylation using the Illumina MethylationEPIC Array. Measurements and Main Results: Significant differences in DNA methylation were noted among subjects with different degrees of asthma severity, as measured by fraction of exhaled nitric oxide, forced expiratory volume, and asthma control test scores. Differences in DNA methylation were annotated to genes that were enriched in pathways related to asthma or T cell function, and included gene ontology categories related to cellular adhesion, developmental pathways, and calcium signaling. Notable genes that were differentially methylated based on asthma severity included RUNX3, several members of the HLA family, PDGFRA, CDH1, CAV1, and NOTCH4. Differences in DNA methylation also varied by exposure to ambient air pollution, with different components of pollution effecting methylation of different groups of genes. Conclusion: These findings demonstrate how adult asthmatics possess widespread differences in the DNA methylation that associated with varying asthma severity and how air pollution might contribute to more severe asthma via changes in DNA methylation.
2024-07-31 | GSE226257 | GEO
Project description:In the present study, we investigate pulmonary transcriptional responses in mice following exposure in situ to ambient air in a heavily polluted urban environment. Mature C57BL/CBA male mice were caged in sheds located in an urban area near two working steel mills and a major highway in Hamilton, Ontario, Canada. Control mice were housed in the same environment but received only high-efficiency particle-filtered air. Whole lung tissues were collected from mice exposed for 3 weeks, 10 weeks or for 10 weeks followed by 6 weeks in the laboratory (16 weeks total). DNA microarrays were used to explore changes in pulmonary gene expression in mice breathing ambient air versus HEPA-filtered air. Transcriptional profiling revealed changes in the expression of genes implicated in the lipid droplet synthesis pathway (plin, dgat2, lpl, s3-12, agpat2), antioxidants (ucp1). We postulate that exposure to particulate matter adsorbed with polycyclic aromatic hydrocarbons triggers lipid droplet synthesis (holding depots for lipids and malformed/excess proteins tagged for degradation) in the lungs, which act to sequester particulates adsorbed with toxic chemicals. Increased lipid droplet synthesis could potentially lead to endogenous/stressor-induced synthesis of reactive oxygen species and activation of antioxidant mechanisms. Further investigation into the stimulation of lipid droplet synthesis in the lung in response to air pollution is warranted in order to better understand these mechanistic changes and the resulting health implications.
2013-09-30 | GSE41698 | GEO
Project description:Comparison of genome-wide gene expression between humans living in areas of high levels of air pollution and less polluted areas. Keywords: Comparison of genome-wide gene expression between different conditions
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Project description:SINERGIA-Phyllosphere bacteria and air pollution
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Project description:The study comprises of 24 subjects that have been exposed to high and low Traffic-related air pollution.
2022-01-01 | GSE125647 | GEO
Project description:Air pollutants including particulate matter (PM) and chemicals adsorbed onto PM pose a serious threat to human health. In this study, we analyzed the ability of PM to induce diverse gene expression profile modulation after chronic exposure in subjects living in two regions of the Czech Republic differing in levels and sources of the air pollution. We also considered impact of different seasonal conditions on concentrations and compositions of PM. Blood samples of 312 subjects from polluted Ostrava city and 154 controls from Prague city were collected in winter 2009, summer 2009 and winter 2010. The highest concentrations of air pollutants were detected in winter 2010 when the subjects were exposed to: PM of aerodynamic diameter < 2.5 M-BM-5m (70 vs. 44.9 M-BM-5g/m3); benzo[a]pyrene (9.02 vs. 2.56 ng/m3) and benzene (10.2 vs. 5.5 M-BM-5g/m3) in Ostrava and Prague, respectively. Global gene expression analysis of total RNA extracted from leukocytes was performed using whole genome microarrays (Illumina). The expression of selected genes was verified by quantitative real-time PCR (qRT-PCR). Despite lower concentrations of air pollutants we found a higher number of differentially expressed genes and affected KEGG pathways in subjects from Prague. In both locations we observed differences between seasons. The qRT-PCR analysis showed a significant decrease in expression of APEX, ATM, FAS, GSTM1, IL1B and RAD21 in subjects from Ostrava, in a comparison of winter 2010 and summer 2009. In Prague, an increase in gene expression was observed for GADD45A and PTGS2. In conclusion, high concentrations of pollutants in Ostrava do not increase the number of differentially expressed genes. This may be explained by adaption of humans to chronic exposure to air pollution. Total RNA was extracted from leukocytes of total of 154 control subjects and 312 subjects exposed to heavy air pollution. The samples were collected in three seasons (winter 2009, summer 2009, winter 2010) with different levels of air pollution. Most of the subjects were sampled repeatedly; however, some of them joined the study in summer 2009 or winter 2010.
2014-08-27 | E-GEOD-60767 | biostudies-arrayexpress
Project description:In the present study, we investigate pulmonary transcriptional responses in mice following exposure in situ to ambient air in a heavily polluted urban environment. Mature C57BL/CBA male mice were caged in sheds located in an urban area near two working steel mills and a major highway in Hamilton, Ontario, Canada. Control mice were housed in the same environment but received only high-efficiency particle-filtered air. Whole lung tissues were collected from mice exposed for 3 weeks, 10 weeks or for 10 weeks followed by 6 weeks in the laboratory (16 weeks total). DNA microarrays were used to explore changes in pulmonary gene expression in mice breathing ambient air versus HEPA-filtered air. Transcriptional profiling revealed changes in the expression of genes implicated in the lipid droplet synthesis pathway (plin, dgat2, lpl, s3-12, agpat2), antioxidants (ucp1). We postulate that exposure to particulate matter adsorbed with polycyclic aromatic hydrocarbons triggers lipid droplet synthesis (holding depots for lipids and malformed/excess proteins tagged for degradation) in the lungs, which act to sequester particulates adsorbed with toxic chemicals. Increased lipid droplet synthesis could potentially lead to endogenous/stressor-induced synthesis of reactive oxygen species and activation of antioxidant mechanisms. Further investigation into the stimulation of lipid droplet synthesis in the lung in response to air pollution is warranted in order to better understand these mechanistic changes and the resulting health implications. Mature male C57BL/6 x CBA F1 hybrid mice were exposed to either HEPA-filtered or ambient air in Hamilton, ON, Canada. Animals were exposed starting May 14, 2004 for 3 weeks (3wk), 10 weeks (10wk), or for 10 weeks followed by 6 weeks of recovery (16wk). Each treatment group consisted of five mice, for a total of 30 mice. Total RNA was isolated from a random section of the whole lung using TRIzol reagent (Invitrogen) and purified using the RNeasy Mini Kit (Qiagen). RNA quality was confirmed by UV spectrophotometry and using an Agilent Bioanalyzer. Total RNA (200 ng) from HEPA-filtered air or whole air-exposed mice and Universal Mouse Reference RNA (Stratagene) were used to synthesize double-stranded cDNA and cyanine-labelled cRNA according to the manufacturer's instructions (Agilent Linear Amplification Kits, Agilent Technologies). Biological samples were labelled with Cy5 dye while the commercially available Stratagene mouse reference RNA was labelled with Cy3 dye. At each of the three time points, ambient air-exposed samples and HEPA-filtered samples were hybridized to Agilent microarrays. Arrays were washed, and scanned on an Agilent G2505B scanner. Data were acquired using the Agilent Feature Extraction software version 9.5.3.1.
2013-09-30 | E-GEOD-41698 | biostudies-arrayexpress