SINERGIA-Phyllosphere bacteria and air pollution
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ABSTRACT:
PROVIDER: PRJEB28871 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Arthrobacter chlorophenolicus A6 is a 4-chlorophenol degrading soil bacterium with high phyllosphere colonization capacity. Till now the genetic basis for the phyllosphere competency of Arthrobacter or other pollutant-degrading bacteria is uncertain. We investigated global gene expression profile of A. chlorophenolicus grown in the phyllosphere of common bean (Phaseolus vulgaris) compared to growth on agar surfaces.
2013-06-21 | GSE48198 | 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
2008-04-17 | GSE7543 | GEO
Project description:Arthrobacter chlorophenolicus A6 is a 4-chlorophenol degrading soil bacterium with high phyllosphere colonization capacity. Till now the genetic basis for the phyllosphere competency of Arthrobacter or other pollutant-degrading bacteria is uncertain. We investigated global gene expression profile of A. chlorophenolicus grown in the phyllosphere of common bean (Phaseolus vulgaris) compared to growth on agar surfaces. We designed transcriptome arrays and investigated which genes had different transcript levels in the phyllosphere of common bean (Phaseolus vulgaris) as compared to agar surfaces. Since water availability is considered an important factor in phyllosphere survival and activity, we included both high and low relative humidity treatments for the phyllosphere-grown cells. In addition, we determined the expression profile under pollutant exposure by the inclusion of two agar surface treatments, i.e. with and without 4-chlorophenol.
2013-06-21 | E-GEOD-48198 | biostudies-arrayexpress
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:Comparison of genome-wide gene expression between humans living in areas of high levels of air pollution and less polluted areas. Experiment Overall Design: The study investigated differential gene expression in peripheral blood from 23 children and 12 adults from a region of residence with high levels of air pollution as compared to 24 children and 12 adults from a less-polluted area.Two conditions: living in the polluted or in the less-polluted area. One individual per array, hybridized against a common reference sample
2008-06-15 | E-GEOD-7543 | biostudies-arrayexpress
Project description:Atopic dermatitis is increasing worldwide, correlating with air pollutions. Various organic components of pollutants activate transcription factor AhR (aryl-hydrocarbon receptor). We have established AhR-CA mice, whose keratinocytes express constitutive-active AhR, and these mice developed atopic dermatitis-like frequent scratching and allergic inflammation. In this study we performed ChIP-seq analyses and identified keratinocyte-specific AhR target genes, including inflammatory cytokines Tslp and IL33, and neurotrophic factor Artemin. While AhR-CA mice exhibited epidermal hyperinnervation and alloknesis leading to hypersensitivity to pruritus, blockade of Artemin alleviated these phenotypes. AhR-CA mice showed scratching-induced barrier insufficiency and enhanced sensitization to epicutaneously-applied antigens, recapitulating human atopic dermatitis. Consistently, AhR activation and Artemin expression was detected in the epidermis of atopic dermatitis patients and keratinocytes exposed to air pollutants. Thus, AhR in keratinocytes senses the environmental stimuli and responds to them through moderating inflammation. We propose a mechanism in which air pollution induces atopic dermatitis through AhR activation.
2016-11-13 | GSE72449 | GEO
Project description:Empirical evidence from both animals and humans suggest that PM2.5 (particulate matter < 2.5μm) exposure accelerates a variety of non-communicable diseases (NCDs) including Type 2 diabetes. We investigated whether chronic exposure to ambient air pollution (PM2.5), disrupts circadian rhythm to facilitate metabolic insulin resistance and compared the impact of inhaled ambient PM2.5 alone or in combination with continuous light exposure (LL). Exposure to PM2.5 induced peripheral IR, disrupted circadian steroid release, reduced peak oxygen consumption and altered brown adipose 18Ffluorodeoxyglucose uptake on PET imaging. These findings were identical to that seen with LL with no additive interaction between PM2.5 and LL. Transcriptome profiles in the liver revealed a number of differentially expressed circadian genes Bmal1 (Arntl/Npas2), Period (Per) and Cryptochrome (Cry) in response to PM2.5. Alteration in chromatin accessibility in circadian targets was observed with PM2.5 by Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) while chromatin immunoprecipitation (ChIP) analysis, showed a marked difference in promoter occupancy by p300. Our data suggest a previously unrecognized role of particulate air pollution in promoting circadian disruption and metabolic dysfunction through epigenetic regulation of multiple circadian targets
2020-12-01 | GSE145566 | GEO
Project description:Metabolic Effects of Air Pollution Exposure and Reversibility
| PRJNA608484 | ENA
Project description:While environmental agents such as air pollution have been shown to be causative to diseases, yet limited knowledge exist on their mechanism of action. Here we used RNA-sequencing in combination with specific immunoprecipitation of 8-oxo-7,8-dihydroguanosine (8-oxoG) to identify transcripts accumulating oxidation after exposure to air pollution (derived from the reaction of 790 ppb acrolein, 670 ppb methacrolein, and 4 ppm ozone) in bronchial epithelial BEAS-2B cells. Results from this analysis suggest a functional role of the 8-oxoG modified transcripts after air pollution exposure in pathways that are central regulators of cell metabolism, growth, proliferation and maintenance of cellular structure. This study highlights a critical role for a RNA epitranscriptomics modification that can be used to further characterize biological responses to external stressors once considered indistinguishable.
2020-07-27 | GSE123933 | GEO