Airborne particulate microbiome in Rwanda
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ABSTRACT:
PROVIDER: PRJEB33617 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3446170_1.fastq.gz | Fastqsanger.gz | |||
| ERR3446170_2.fastq.gz | Fastqsanger.gz | |||
| ERR3446180_1.fastq.gz | Fastqsanger.gz | |||
| ERR3446180_2.fastq.gz | Fastqsanger.gz | |||
| ERR3446190_1.fastq.gz | Fastqsanger.gz |
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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
Project description:The aim of the present study was to characterize a common and unique signalling pathways associated to two seasonal particulate matter (PM) (winter PM2.5 and summer PM10) in human bronchial BEAS-2B cells by mean of a global transcriptomic profiling (including genes and miRNA) and the investigation of selected pathways at protein level.
2016-05-26 | E-MTAB-3629 | biostudies-arrayexpress
Project description:The aim of the present study was to characterize a common and unique signalling pathways associated to two seasonal particulate matter (PM) (winter PM2.5 and summer PM10) in human bronchial BEAS-2B cells by mean of a global transcriptomic profiling (including genes and miRNA) and the investigation of selected pathways at protein level.
2016-05-26 | E-MTAB-3630 | biostudies-arrayexpress
Project description:Particulate matter10 (PM10) can induce airway inflammation and fibrosis. Chitinase-1 is recently known to have key roles in inflammation and fibrosis. We aimed to investigate the effects of chitinase-1 inhibitor in PM10-treated murine models. PM10 and/or OVA-induced airway inflammation and fibrosis murine models were well established. CPX and dexamethasone ameliorated PM10 or PM10/OVA-induced airway hyper-responsiveness, airway inflammation, and fibrosis. CPX and dexamethasone also reduced levels of various inflammatory markers including chitinase-1 in lung homogenates. PM10 and OVA also induced extreme changes of mRNA expression. CPX and dexamethasone decreased levels of mRNA expression especially associated with inflammation and immune regulation. They also significantly regulated asthma and asthma related pathway including JACK-STAT signaling pathway.Chitinase-1 suppression by CPX can regulate PM10-induced and aggravated airway inflammation and fibrosis via various signaling pathway.
2023-01-05 | GSE222111 | GEO
Project description:Objectives: To explore the molecular mechanisms of PM2.5-induced dysfunction in human corneal epithelial cells (HCECs). Methods: RNA-Seq was performed to identify the differentially expressed genes (DEGs) in PM2.5-exposed HCECs compared to unexposed condition, which was followed by validation via real-time PCR (qRT-PCR). Results: A total of 434 DEGs—240 up-regulated and 194 down-regulated—were identified in PM2.5-exposed HCECs rather than unexposed HCECs. The expression of a few genes related to proliferation, inflammation, and aryl hydrocarbon stimulation were significantly altered by PM2.5 exposure, which may contribute to PM2.5-related corneal diseases. Conclusion: The present study identified the altered expression of hundreds of genes in HCECs exposed to PM2.5, which suggests the importance of PM2.5 for cornea health.
2022-08-01 | GSE135262 | GEO
Project description:Particulate matter PM2.5 Raw sequence reads
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Project description:Background: Mast cells play an important role in allergic responses and persistently exposure to environmental fine particulate matter (PM2.5) exacerbates allergic diseases,but the details remain elucidative. Conclusions: PM2.5 regulates ROS production through Gadd45b/MEKK4/JNK pathway, facilitating IgE-mediated mast cell activation.
2021-01-12 | GSE164537 | GEO
Project description:Genome-wide analysis of lncRNA expression profiles in COPD rat model exposed by cigarette smoking (CS) and fine particulate matter (PM2.5). Goal was to explore the differences and similarities lncRNAs expression in rats model of COPD exposed by CS and PM2.5.
2021-06-21 | GSE178513 | GEO
Project description:Open tenotomy of the Achilles tendon of 6 rats was performed. The animals were divided into two groups according to exposure of PM2.5 (particulate matter less than 2.5 µm): control group (Non-PM group) or PM exposure group (PM group). After 6 weeks of PM exposure, the tendon RNA was extracted and anlyzed.
2022-08-03 | GSE200463 | GEO