Toxicological Transcriptome of Human Airway Constructs After Exposure to Indoor Air Particulate Matter: In Search of Relevant Pathways of Moisture Damage -Associated Health Effects
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ABSTRACT:
PROVIDER: PRJNA734174 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14698900_1.fastq.gz | Fastqsanger.gz | |||
| SRR14698900_2.fastq.gz | Fastqsanger.gz | |||
| SRR14699000_1.fastq.gz | Fastqsanger.gz | |||
| SRR14699000_2.fastq.gz | Fastqsanger.gz | |||
| SRR14698901_1.fastq.gz | Fastqsanger.gz |
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Project description:Background - Multiple health effects are associated with moisture damage in buildings. Studies explaining these associations and cell-level mechanisms behind the observed health effects are urgently called for. Objectives - Alongside general toxicological markers, we focused on characterizing gene expression in human airway epithelium after exposure to indoor air particulate matter (PM) sampled from houses with and without moisture damage. Methods - We performed detailed technical building inspections in 25 residential houses and categorized them based on the detection of moisture damages and the probability of occupant exposure. PM sampling was complemented by microbiological and volatile organic compound assessment. We exposed airway constructs to three doses (1:16, 1:8, 1:4) of PM from moisture-damaged (index) and non-moisture-damaged (reference) houses. The RNA of exposed constructs was sequenced targeting toxicology -related genes. We did groupwise comparisons between index and reference houses and pairwise comparisons in matched index/reference houses. We analyzed general toxicological markers and imaged the constructs with electron microscopy. Results - In pairwise comparison, several genes were differentially expressed. Genes related to multiple toxicological pathways were highlighted, while none of the genes was consistently expressed in all the comparisons. In groupwise comparison, CYP1A1 was statistically significantly over-expressed in index houses at all doses (dose 1:16 log2FC = 0.007, padj = 0.03; dose 1:8 log2FC = 0.077, padj = 0.018; dose 1:4 log2FC = 0.270, padj = 0.002) and NFKB1 at the highest dose 1:4 (log2FC = 0.124, padj = 0.029). General toxicological markers did not separate the index/reference houses. Discussion - The exposure to PM from index houses activates toxicology -related genes in airway constructs. While differential expression was not consistent among all the index/reference pairs, possibly due to compositional differences of bioactive particles, our study highlights CYP1A1 and NFKB1 as potential targets in moisture damage -associated cellular responses.
2022-04-27 | GSE175878 | GEO
Project description:There is a need for toxicity tests capable of recognizing indoor environments with compromised air quality, especially in the context of moisture damage. One of the key issues is sampling, which should both provide meaningful material for analyses and fulfill requirements imposed by practitioners using toxicity tests for health risk assessment. We aimed to evaluate different existing methods of sampling indoor particulate matter (PM) to develop a suitable sampling strategy for a toxicological assay. During three sampling campaigns in moisture-damaged and non-damaged school buildings, we evaluated one passive and three active sampling methods: the Settled Dust Box (SDB), the Button Aerosol Sampler, the Harvard Impactor and the National Institute for Occupational Safety and Health (NIOSH) Bioaerosol Cyclone Sampler. Mouse RAW264.7 macrophages were exposed to particle suspensions and cell metabolic activity (CMA), production of nitric oxide (NO) and tumor necrosis factor (TNFα) were determined after 24 h of exposure. The repeatability of the toxicological analyses was very good for all tested sampler types. Variability within the schools was found to be high especially between different classrooms in the moisture-damaged school. Passively collected settled dust and PM collected actively with the NIOSH Sampler (Stage 1) caused a clear response in exposed cells. The results suggested the higher relative immunotoxicological activity of dust from the moisture-damaged school. The NIOSH Sampler is a promising candidate for the collection of size-fractionated PM to be used in toxicity testing. The applicability of such sampling strategy in grading moisture damage severity in buildings needs to be developed further in a larger cohort of buildings.
| S-EPMC5015124 | biostudies-literature
Project description:Response pattern of soil prokaryotic community under an artificial moisture gradient
| PRJEB19528 | ENA
Project description:Leaf rate elongation is extremely sensitive to soil water status. Global gene expression of the leaf elongation zone was profiled at three different levels of soil moisture in two genotypes. Leaf elongation in IR64 is more sensitive to decreased soil moisture than in moroberekan.
2012-09-26 | GSE41159 | GEO
Project description:Background: In classrooms high concentrations of particulate matter PM10 were measured. It is unknown whether the hazard of indoor particles is similar to that of the better studied outdoor particles. This study therefore analyzed adverse biological effects of classroom in comparison to outdoor PM10. Methods: Samples were taken from six schools during teaching hours. Genome-wide gene expression in human bronchial BEAS-2B epithelial cells was analyzed, and regulated genes were verified by quantitative PCR. Polycyclic aromatic hydrocarbons (PAH), endotoxin, and cat allergen Fel d 1 were analyzed with standard methods. Enhancement of allergic reactivity by PM10 was confirmed with CD63 upregulation in human primary basophils. Acceleration of human blood coagulation was determined with supernatants of PM10-exposed human peripheral blood monocytes. Results: Indoor PM10 induced SERPINB2 (involved in blood coagulation) and inflammatory genes (like CXCL6, CXCL1, IL6, IL8, all p<0.001). Outdoor PM10 induced xenobiotic metabolizing enzymes (CYP1A1, CYP1B1, TIPARP, all p<0.001). The induction of inflammatory genes by indoor PM10 could be explained by endotoxin (indoor 128.5±42.2EU/mg versus outdoor 13.4±21.5EU/mg, p<0.001), the induction of CYP by outdoor PAH (indoor 8.3±4.9ng/mg versus outdoor 16.7±15.2ng/mg, p<0.01). The induction of SERPINB2 was confirmed by a more rapid human blood coagulation (p<0.05). Indoor PM10 had no effect on the allergic reactivity from human primary basophils, except in cat allergic individuals. This was explained by varying Fel d 1 concentrations in indoor PM10 (p<0.001). Conclusions: Indoor PM10, compared to outdoor PM10, was 6 times higher, had a different composition, and on an equal weight basis induced more inflammatory and allergenic reactions, and accelerated blood coagulation. Outdoor PM10 had significantly lower effects, but induced detoxifying enzymes. Therefore, preliminary interventions for the reduction of classroom PM10 seem reasonable, perhaps by intensified ventilation.
2012-12-21 | GSE34607 | GEO
Project description:Background: In classrooms high concentrations of particulate matter PM10 were measured. It is unknown whether the hazard of indoor particles is similar to that of the better studied outdoor particles. This study therefore analyzed adverse biological effects of classroom in comparison to outdoor PM10. Methods: Samples were taken from six schools during teaching hours. Genome-wide gene expression in human bronchial BEAS-2B epithelial cells was analyzed, and regulated genes were verified by quantitative PCR. Polycyclic aromatic hydrocarbons (PAH), endotoxin, and cat allergen Fel d 1 were analyzed with standard methods. Enhancement of allergic reactivity by PM10 was confirmed with CD63 upregulation in human primary basophils. Acceleration of human blood coagulation was determined with supernatants of PM10-exposed human peripheral blood monocytes. Results: Indoor PM10 induced SERPINB2 (involved in blood coagulation) and inflammatory genes (like CXCL6, CXCL1, IL6, IL8, all p<0.001). Outdoor PM10 induced xenobiotic metabolizing enzymes (CYP1A1, CYP1B1, TIPARP, all p<0.001). The induction of inflammatory genes by indoor PM10 could be explained by endotoxin (indoor 128.5M-BM-142.2EU/mg versus outdoor 13.4M-BM-121.5EU/mg, p<0.001), the induction of CYP by outdoor PAH (indoor 8.3M-BM-14.9ng/mg versus outdoor 16.7M-BM-115.2ng/mg, p<0.01). The induction of SERPINB2 was confirmed by a more rapid human blood coagulation (p<0.05). Indoor PM10 had no effect on the allergic reactivity from human primary basophils, except in cat allergic individuals. This was explained by varying Fel d 1 concentrations in indoor PM10 (p<0.001). Conclusions: Indoor PM10, compared to outdoor PM10, was 6 times higher, had a different composition, and on an equal weight basis induced more inflammatory and allergenic reactions, and accelerated blood coagulation. Outdoor PM10 had significantly lower effects, but induced detoxifying enzymes. Therefore, preliminary interventions for the reduction of classroom PM10 seem reasonable, perhaps by intensified ventilation. For genome-wide gene expression analysis, BEAS-2B cells (passage 41) were incubated with 10M-BM-5g/ml PM10 (school 4 indoor and outdoor) for 4, 10 or 24h, all in triplicate. experiment type : time course
2012-12-21 | E-GEOD-34607 | biostudies-arrayexpress