Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA269614 | ENA |
REPOSITORIES: ENA
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Project description:Human BEAS-2B bronchial epithelial cells were exposed directly at the air-liquid interphase towards exhaust gas and particles of a ship engine. The goal was to compare the responses towards different fuel combustions. The engine run either on diesel fuel (DF) or on Heavy Fuel Oil (HFO).
2015-02-01 | GSE63962 | GEO
Project description:Human BEAS-2B bronchial epithelial cells were exposed directly at the air-liquid interphase towards exhaust gas and particles of a ship engine. The goal was to compare the responses towards different fuel combustions. The engine run either on diesel fuel (DF) or on Heavy Fuel Oil (HFO). The lung cells were exposed 3 times to each combustion aerosol (DF or HFO). The duration of the exposure was 4h. The cells were seeded into transwell-inserts 24h before exposure. Within each exposure 3 transwell-inserts were exposed to the complete aerosol and 3 transwell-inserts were exposed to the filtered aerosol. Effects of the complete aerosol were referenced against the filtered aerosol to determine the effects of the aerosol particles.
2015-02-01 | E-GEOD-63962 | biostudies-arrayexpress
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
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. 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.
2012-03-01 | E-GEOD-34025 | biostudies-arrayexpress
Project description:We performed a single-cell transcriptome analysis of colon monocytes and macrophages in 2 control mice and 2 mice orally treated with diesel exhaust particles.
2023-07-12 | GSE133406 | GEO
Project description:We performed a single-cell transcriptome analysis of colon monocytes and macrophages in 2 control mice and 2 mice orally treated with diesel exhaust particles.
2023-06-30 | GSE131432 | GEO
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
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
Project description:There is an emerging concern that particulate air pollution increases the risk of cranial nerve disease onset. Small nanoparticles, mainly derived from diesel exhaust particles reach the olfactory bulb by their nasal depositions. It has been reported that diesel exhaust inhalation causes inflammation of the olfactory bulb and other brain regions. However, these toxicological studies have not evaluated animal rearing environment. We hypothesized that rearing environment can change mice phenotypes and thus might alter toxicological study results. In this study, we exposed mice to diesel exhaust inhalation at 90 micro g/m3, 8 hours/day, for 28 consecutive days after rearing in a standard cage or environmental enrichment conditions. Microarray analysis found that expression levels of 112 genes were changed by diesel exhaust inhalation. Functional analysis using Gene Ontology revealed that the dysregulated genes were involved in inflammation and immune response. This result was supported by pathway analysis. Quantitative RT-PCR analysis confirmed 10 genes. Interestingly, background gene expression of the olfactory bulb of mice reared in a standard cage environment was changed by diesel exhaust inhalation, whereas there was no significant effect of diesel exhaust exposure on gene expression levels of mice reared with environmental enrichment. The results indicate for the first time that the effect of diesel exhaust exposure on gene expression of the olfactory bulb was influenced by rearing environment. Rearing environment, such as environmental enrichment, may be an important contributive factor to causation in evaluating still undefined toxic environmental substances such as diesel exhaust. RNA sample was taken from olfactory bulb of 56-day-old mouse received diesel exhaust (DE) inhalation at 90 micro g/m3, 8 hours/day, for 28 consecutive days, while control RNA was taken from mouse received clean air, after rearing in a standard cage or environmental enrichment conditions. Comparisons among groups were made by one-color method with normalized data from Cy3 channels for data analysis.
2013-04-18 | E-GEOD-46163 | biostudies-arrayexpress
Project description:MicroRNA microarray profiling of Murine lung exposed to diesel exhaust
2023-12-01 | GSE226885 | GEO