{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"omics_type":["Metabolomics","Unknown","Transcriptomics","Genomics","Proteomics"],"submitter":["Roland Lang"],"study_type":["transcription profiling by array"],"organism":["Homo sapiens"],"species":["Homo sapiens"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-GEOD-34607"],"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"],"repository":["biostudies-arrayexpress"],"sample_protocol":["Growth Protocol - Human immortalized bronchial epithelial BEAS-2B cells were cultured in bronchial epithelial cell basal medium (BEBMM-.; Bronchial Epithelial Cell Basal Medium; CloneticsM-., Lonza Inc., Walkersville, USA) with 100 units/ml penicillin/streptomycin and bovine pituitary extract, hydrocortisone, hEGF, epinephrine, transferrin, insulin, retinoic acid, triiodothyronine in manufacturer-recommended concentrations (BEGMM-. SingleQuotsM-., Lonza). To improve cell adherence, culture plates were pre-coated with 0.01 mg/ml fibronectin, 0.03 mg/ml bovine collagen Type 1 and 0.01 mg/ml BSA. Exponential growing cells were sustained at 37M-0C, 90% relative humidity and 5% CO2.","Sample Processing - For genome-wide gene expression analysis BEAS-2B cells (passage 41) were incubated with 10M-5g/ml PM10 (school 4 indoor and outdoor) for 4, 10 or 24h, all in triplicate.","Labeling - Per sample, 200 ng total RNA was processed using AmbionM-bM-^@M-^Ys MessageAmp II Biotin Enhanced labeling kit according to the manufacturerM-bM-^@M-^Ys instructions.","Nucleic Acid Extraction - Subsequentially total RNA was extracted (RNeasy Micro Kit; Qiagen) and its concentration (Nanodrop, PeqLab) and quality (Bioanalyzer, Agilent Inc.) were tested.","Hybridization - Biotinylated cRNA was hybridized on Affymetrix HG U133A 2.0 GeneChips, that were stained, washed and scanned following Affymetrix standard procedures."],"figure_sub":["MIAME Score","Raw Data","Organization","Assays and Data","Processed Data","MAGE-TAB Files","Array Designs"],"pubmed_authors":["Jeroen Buters","Roland Lang","Sebastian Oeder"],"data_protocol":["Feature Extraction - The probe level data (CEL files) were processed for global normalization and generation of expression values using the robust multi-array average algorithm (RMA) of the M-bM-^@M-^\\affy packageM-bM-^@M-^] in the R software environment (http://www.R-project.org).","Assay Data Transformation - ID_REF =  VALUE = RMA normalized","Image Adquisition - Biotinylated cRNA was hybridized on Affymetrix HG U133A 2.0 GeneChips, that were stained, washed and scanned following Affymetrix standard procedures."],"additional_accession":[]},"is_claimable":false,"name":"Airborne particulate matter affects gene expression in BEAS-2B bronchial epithelial cells.","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","dates":{"release":"2012-12-21T00:00:00Z","modification":"2023-08-19T13:00:34.927Z","creation":"2022-03-10T09:08:21.7Z"},"accession":"E-GEOD-34607","cross_references":{"GEO":["GSE34607"],"EFO":["EFO_0002768"]}}