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Unknown,Transcriptomics,Genomics,Proteomics

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Traffic-related Particulate Matter Upregulates Allergic Responses by a Notch-pathway Dependent Mechanism

ABSTRACT: The mechanisms by which diesel exhaust particles act as an adjuvant are unknown. We hypothesized that these would be mediated through monocyte interactions with DEP. We sought to identify pathways with a role in inflammation or other signaling mechanisms that might demonstrate the mechanism of response to DEP. Cultured human monocytes from healthy donors were cultured in the presence or absence of diesel exhaust particles. RNA was extracted following culture to determine changes in gene expression pathways.

ORGANISM(S): Homo sapiens

SUBMITTER: Sean McGhee

PROVIDER: E-GEOD-34025 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:The mechanisms by which diesel exhaust particles act as an adjuvant are unknown. We hypothesized that these would be mediated through monocyte interactions with DEP. We sought to identify pathways with a role in inflammation or other signaling mechanisms that might demonstrate the mechanism of response to DEP.

2012-03-01 | GSE34025 | GEO

Differential Transcriptional Changes in Mice Exposed to Chemically Distinct Diesel Samples

Project description:Epidemiological studies have linked exposure to ambient particulate matter (PM) with increased asthmatic symptoms. Diesel exhaust particles (DEP) are a predominant source of vehicle derived ambient PM, and experimental studies have demonstrated that they may have adjuvant potential when given with an antigen. We previously compared 3 DEP samples: N-DEP, A-DEP, and C-DEP in a murine ovalbumin (OVA) mucosal sensitization model and reported the adjuvant activity to be: C-DEP ? A-DEP > N-DEP. The present study analyzed gene expression changes from the lungs of these mice. Transcription profiling demonstrated that all the DEP samples altered cytokine and toll-like receptor pathways regardless of type, with or without antigen sensitization. Further analysis of DEP exposure with OVA showed that all DEP treatments altered networks involved in immune and inflammatory responses. The A- and C-DEP/OVA treatments induced differential expression of apoptosis pathways in association with stronger adjuvant responses, while expression of cell cycle control and DNA damage pathways were also altered in the C-DEP/OVA treatment. This comprehensive approach using gene expression analysis to examine changes at a pathway level provides detailed information on events occurring in the lung after DEP exposure, and confirms that the most bioactive sample induced many more individual genes and changes in immuno-regulatory and homeostatic pathways. Female BALB/C mice (8-10 weeks old) were randomly divided into 8 treatment groups containing 3 mice each and exposed to saline, 20 ug ovalbumin, 150 ug diesel exhaust particles (either C-DEP, A-DEP, or N-DEP), or diesel exhaust particles + ovalbumin by intranasal instillation on Days 0 and 13 and necropsied 18 hrs latter.

2010-07-10 | E-GEOD-22357 | biostudies-arrayexpress

Proteomic analysis reveals activation of platelet- and fibrosis-related pathways in hearts of ApoE-/- mice exposed to diesel exhaust particles

Project description:Air pollution is an environmental risk factor linked to multiple human diseases including cardiovascular diseases (CVDs). While particulate matter (PM) emitted by diesel exhaust damages multiple organ systems, heart disease is one of the most severe pathologies affected by PM. However, the in vivo effects of diesel exhaust particles (DEP) on the heart and the molecular mechanisms of DEP-induced heart dysfunction have not been investigated. In the current study, we attempted to identify the proteomic signatures of heart fibrosis caused by diesel exhaust particles (DEP) in CVDs-prone apolipoprotein E knockout (ApoE-/-) mice model using tandem mass tag (TMT)-based quantitative proteomic analysis. DEP exposure induced mild heart fibrosis in ApoE-/- mice compared with severe heart fibrosis in ApoE-/- mice that were treated with CVDs-inducing peptide, angiotensin II. TMT-based quantitative proteomic analysis of heart tissues between PBS- and DEP-treated ApoE-/- mice revealed significant upregulation of proteins associated with platelet activation and TGFβ-dependent pathways. Our data suggest that DEP exposure could induce heart fibrosis, potentially via platelet-related pathways and TGFβ induction, causing cardiac fibrosis and dysfunction.

2023-12-09 | PXD045029 | Pride

DNA methylation changes in A549 cells after four weeks of exposure to 30 μg/ml diesel exhaust particles.

Project description:Diesel exhaust particles (DEP), which contain hazardous compounds, are emitted during the combustion of diesel. As approximately one-third of the vehicles worldwide use diesel, there are growing concerns on the risks posed by DEP to human health. Long-term exposure to DEP is associated with airway hyperresponsiveness, pulmonary fibrosis, and inflammation; however, the molecular mechanisms behind the effects of DEP on the respiratory tract are poorly understood. Such mechanisms can be addressed by examining transcriptional and DNA methylation changes. In this study, we investigated the effect of 4 weeks exposure to 30 μg/ml DEP on DNA methylation levels in A549 cells.

2024-08-05 | GSE267215 | GEO

Identification of a dose of diesel exhaust particles that is sufficient to induce significant DNA methylation changes in A549 cells after four weeks of exposure.

Project description:Diesel exhaust particles (DEP), which contain hazardous compounds, are emitted during the combustion of diesel. As approximately one-third of the vehicles worldwide use diesel, there are growing concerns on the risks posed by DEP to human health. Long-term exposure to DEP is associated with airway hyperresponsiveness, pulmonary fibrosis, and inflammation; however, the molecular mechanisms behind the effects of DEP on the respiratory tract are poorly understood. Such mechanisms can be addressed by examining transcriptional and DNA methylation changes. In this study, we investigated DEP dose sufficient to induce significant DNA methylation changes after four weeks of exposure.

2024-08-05 | GSE267214 | GEO

Transcriptional changes in A549 cells after four weeks of exposure to 30 μg/ml diesel exhaust particles measured by RNA-seq.

2024-08-05 | GSE267213 | GEO

Transcriptional changes in A549 cells after four weeks of exposure to 30 μg/ml diesel exhaust particles measured by Agilent SurePrint G3 Human Gene Expression Microarray.

2024-08-05 | GSE267216 | GEO

In vitro transformation of human bronchial epithelial cells by diesel exhaust particles

Project description:The potential of diesel exhaust particles (DEP) to transform human bronchial epithelial cells (HBEC3) was investigated and a stably transformed cell line (T2-HBEC3) was established. Short-term DEP exposure experiments adds information of immunomodulatory effect markers and differences in susceptibility between normal and sensitized bronhial epithelial cells of the human lung.

2017-11-30 | GSE107481 | GEO

Pulmonary effects of inhaled diesel particles in rats

Project description:The pulmonary response to inhalation exposure to diesel exhaust particles (DEP) was investigated in a rat model. Adult male Sprague-Dawley rats were exposed by whole-body inhalation to air or an aerosol containing DEP at concentrations of 200 or 1000 mg/m3, 6 hours/day for 4 days. The control and DEP-exposed rats were euthanized at post-exposure time intervals of 1, 7, or 27 days and pulmonary inflammatory, cytotoxic and oxidant responses were determined. Analysis of bronchoalveolar lavage parameters of toxicity such as lactate dehydrogenase activity, oxidant generation, and inflammation did not reveal any significant pulmonary toxicity in the DEP-exposed rats. The lung gene expression profiles did not change significantly in the DEP exposed rats compared with the controls. The data obtained from the present study demonstrated that DEP inhalation exposure under the conditions employed in the present study did not result in any significant lung toxicity in the rats.

2022-12-31 | GSE152720 | GEO

Effect of Diesel Exhaust Particles in Normal Human Embryonic Lung Cell (WI-38) Line

Project description:We performed RNA sequencing to identify genes and pathways induced by Diesel exhaust particles exposure in WI-38 cells.

2021-02-14 | GSE166729 | GEO