Ontology highlight
ABSTRACT:
PROVIDER: PRJNA815337 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18305213_1.fastq.gz | Fastqsanger.gz | |||
| SRR18305213_2.fastq.gz | Fastqsanger.gz | |||
| SRR18305214_1.fastq.gz | Fastqsanger.gz | |||
| SRR18305214_2.fastq.gz | Fastqsanger.gz | |||
| SRR18305215_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Previous reports showed that cigarette smoke exposed normal-appearing airways in phenotypically lung cancer-free smokers carry alterations that are characteristic of tumors – suggestive of an airway field of injury. Very little is known of the effects of the chronic consumption of other forms of tobacco, such as waterpipe smoke (WPS), on lung pathobiology. Here we studied normal-appearing airway brushings from waterpipe smokers and those who were not exposed to WPS. We find that WPS elicits a molecular field of injury with gene programs that are pertinent to lung carcinogenesis.
2022-07-13 | GSE197653 | GEO
Project description:Waterpipe (also called hookah, shisha, or narghile) smoking is a common form of tobacco use in the Middle East. Its use is becoming more prevalent in Western societies, especially among young adults as an alternative form of tobacco use to traditional cigarettes. While the risk to cigarette smoking is well documented, the risk to waterpipe smoking is not well defined with limited information on its health impact at the epidemiologic, clinical and biologic levels with respect to lung disease. Based on the knowledge that airway epithelial cell DNA methylation is modified in response to cigarette smoke and in cigarette smoking-related lung diseases, we assessed the impact of light-use water-pipe smoking on DNA methylation of the small airway epithelium (SAE) and whether changes in methylation were linked to the transcriptional output of the cells. Small airway epithelium was obtained from 7 nonsmokers and 7 light-use (2.6 ± 1.7 sessions/wk) waterpipe-only smokers. Genome-wide comparison of SAE DNA methylation of waterpipe smokers to nonsmokers identified 727 probesets differentially methylated (fold-change >1.5, p<0.05) representing 673 unique genes. Dominant pathways associated with these epigenetic changes include those linked to G-protein coupled receptor signaling, aryl hydrocarbon receptor signaling and xenobiotic metabolism signaling, all of which have been associated with cigarette smoking and lung disease. Of the genes differentially methylated, 11.3% exhibited a corresponding significant (p<0.05) change in gene expression with enrichment in pathways related to regulation of mRNA translation and protein synthesis (eIF2 signaling and regulation of eIF4 and p70S6K signaling). Overall, these data demonstrate that light-use waterpipe smoking is associated with epigenetic changes and related transcriptional modifications in the SAE, the cell population demonstrating the earliest pathologic abnormalities associated with chronic cigarette smoking. This study demonstrates that light-use waterpipe smoking in young adults is associated with a broad range of genome-wide DNA methylation-related changes of the SAE impacting a number of genes linked to pathways previously associated with cigarette smoking. Further, many of these methylation-related changes correlate with waterpipe smoking-associated changes in the SAE transcriptome. Together, these data add to the accumulating evidence that waterpipe smoking is harmful, and may lead to lung disease.
2017-06-13 | GSE92661 | GEO
Project description:Waterpipe (also called hookah, shisha, or narghile) smoking is a common form of tobacco use in the Middle East. Its use is becoming more prevalent in Western societies, especially among young adults as an alternative form of tobacco use to traditional cigarettes. While the risk to cigarette smoking is well documented, the risk to waterpipe smoking is not well defined with limited information on its health impact at the epidemiologic, clinical and biologic levels with respect to lung disease. Based on the knowledge that airway epithelial cell DNA methylation is modified in response to cigarette smoke and in cigarette smoking-related lung diseases, we assessed the impact of light-use water-pipe smoking on DNA methylation of the small airway epithelium (SAE) and whether changes in methylation were linked to the transcriptional output of the cells. Small airway epithelium was obtained from 7 nonsmokers and 7 light-use (2.6 ± 1.7 sessions/wk) waterpipe-only smokers. Genome-wide comparison of SAE DNA methylation of waterpipe smokers to nonsmokers identified 727 probesets differentially methylated (fold-change >1.5, p<0.05) representing 673 unique genes. Dominant pathways associated with these epigenetic changes include those linked to G-protein coupled receptor signaling, aryl hydrocarbon receptor signaling and xenobiotic metabolism signaling, all of which have been associated with cigarette smoking and lung disease. Of the genes differentially methylated, 11.3% exhibited a corresponding significant (p<0.05) change in gene expression with enrichment in pathways related to regulation of mRNA translation and protein synthesis (eIF2 signaling and regulation of eIF4 and p70S6K signaling). Overall, these data demonstrate that light-use waterpipe smoking is associated with epigenetic changes and related transcriptional modifications in the SAE, the cell population demonstrating the earliest pathologic abnormalities associated with chronic cigarette smoking. This study demonstrates that light-use waterpipe smoking in young adults is associated with a broad range of genome-wide DNA methylation-related changes of the SAE impacting a number of genes linked to pathways previously associated with cigarette smoking. Further, many of these methylation-related changes correlate with waterpipe smoking-associated changes in the SAE transcriptome. Together, these data add to the accumulating evidence that waterpipe smoking is harmful, and may lead to lung disease.
2017-06-13 | GSE84101 | GEO
Project description:This experiment investigated the response of mouse pulmonary epithelial cells in culture (FE1 cell line) to 3 different brands of cigarette smoke condensate. The three brands represent a full flavour, regular and king-size light cigarettes. These vary in some key chemical consistuents. Brand #1 has the highest tar content. The cells were exposed to two doses: one at approximately 50% cytotoxicity, and the other at approximately 20%. Both doses were clastogenic. The major pathways affected included xenobiotic metabolism, cell cycle, apoptosis, oxidative stress and inflammation. Although brand #1 exhibited the most numbers of genes that were differentially expressed, there did not appear to be any major differences in the expression profiles between the brands. Although some genes did not reach statistical significance, in general there was consistency in the direction of fold changes for genes across all brands.
2012-04-02 | GSE30079 | GEO
Project description:Previous reports showed that cigarette smoke elicits various molecular and immune changes in the lung. Very little is known of the effects of the chronic consumption of other forms of tobacco, such as waterpipe smoke (WPS), on lung pathobiology. Here, we studied the effects of chronic exposure to WPS versus control air on lungs of tumor-prone mice by RNA-sequencing (RNA-Seq). We find that WPS elicits immunomodulatory changes in the lung that are pertinent to carcinogenesis.
2022-07-13 | GSE197994 | GEO
Project description:<p>The study of antimicrobial resistance (AMR) in infectious diarrhea has generally been limited to cultivation, antimicrobial susceptibility testing and targeted PCR assays. When individual strains of significance are identified, whole genome shotgun (WGS) sequencing of important clones and clades is performed. Genes that encode resistance to antibiotics have been detected in environmental, insect, human and animal metagenomes and are known as "resistomes". While metagenomic datasets have been mined to characterize the healthy human gut resistome in the Human Microbiome Project and MetaHIT and in a Yanomani Amerindian cohort, directed metagenomic sequencing has not been used to examine the epidemiology of AMR. Especially in developing countries where sanitation is poor, diarrhea and enteric pathogens likely serve to disseminate antibiotic resistance elements of clinical significance. Unregulated use of antibiotics further exacerbates the problem by selection for acquisition of resistance. This is exemplified by recent reports of multiple antibiotic resistance in Shigella strains in India, in Escherichia coli in India and Pakistan, and in nontyphoidal Salmonella (NTS) in South-East Asia. We propose to use deep metagenomic sequencing and genome level assembly to study the epidemiology of AMR in stools of children suffering from diarrhea. Here the epidemiology component will be surveillance and analysis of the microbial composition (to the bacterial species/strain level where possible) and its constituent antimicrobial resistance genetic elements (such as plasmids, integrons, transposons and other mobile genetic elements, or MGEs) in samples from a cohort where diarrhea is prevalent and antibiotic exposure is endemic. The goal will be to assess whether consortia of specific mobile antimicrobial resistance elements associate with species/strains and whether their presence is enhanced or amplified in diarrheal microbiomes and in the presence of antibiotic exposure. This work could potentially identify clonal complexes of organisms and MGEs with enhanced resistance and the potential to transfer this resistance to other enteric pathogens.</p> <p>We have performed WGS, metagenomic assembly and gene/protein mapping to examine and characterize the types of AMR genes and transfer elements (transposons, integrons, bacteriophage, plasmids) and their distribution in bacterial species and strains assembled from DNA isolated from diarrheal and non-diarrheal stools. The samples were acquired from a cohort of pediatric patients and controls from Colombia, South America where antibiotic use is prevalent. As a control, the distribution and abundance of AMR genes can be compared to published studies where resistome gene lists from healthy cohort sequences were compiled. Our approach is more epidemiologic in nature, as we plan to identify and catalogue antimicrobial elements on MGEs capable of spread through a local population and further we will, where possible, link mobile antimicrobial resistance elements with specific strains within the population.</p>
| phs001260 | dbGaP
Project description:Alternations in gene methylation and other epigenetic changes regulate normal development as well as drive disease progression. Chronic cigarette smoking causes hyper- and hypo-methylation of genes that could contribute to smoking-related diseases. It is unclear whether consumers of non-combustible tobacco, such as moist snuff, also exhibit such perturbations in their methylome. Here, we present global methylation changes relative to non-tobacco consumers in buccal cells collected from smokers (SMK) and moist snuff consumers (MSC). Generally healthy adult male study subjects were recruited into SMK, MSC and Non-Tobacco Consumer (NTC) cohorts (40 subjects/cohort). Global methylation profiling was performed on the Illumina 450K methylation array using buccal cell DNA. A total of 1,252 loci were found to be significantly differentially methylated in tobacco consumers relative to non-tobacco consumers. Overall, the SMK cohort exhibited larger qualitative and quantitative changes relative to MSC. Approximately half of the total number of gene loci, classified as Combustible Tobacco-Related signatures, and a third of the changes, termed Tobacco-Related signatures, were commonly detected in the tobacco consumers. Very few differences were detected between MSC and NTC, and hierarchical clustering of the top 50 significant gene loci suggested that MSC and NTC co-cluster. Consistent with physiological functions of AhR, combustible tobacco drives profound changes in buccal cell methylation status, principally impacting cell development and immune response pathways. These results aid in placing combustible and non-combustible tobacco products along a risk continuum and provide additional insights into the effects of tobacco consumption.
2017-12-01 | GSE94876 | GEO
Project description:This experiment investigated the response of mouse pulmonary epithelial cells in culture (FE1 cell line) to 3 different brands of cigarette smoke condensate. The three brands represent a full flavour, regular and king-size light cigarettes. These vary in some key chemical consistuents. Brand #1 has the highest tar content. The cells were exposed to two doses: one at approximately 50% cytotoxicity, and the other at approximately 20%. Both doses were clastogenic. The major pathways affected included xenobiotic metabolism, cell cycle, apoptosis, oxidative stress and inflammation. Although brand #1 exhibited the most numbers of genes that were differentially expressed, there did not appear to be any major differences in the expression profiles between the brands. Although some genes did not reach statistical significance, in general there was consistency in the direction of fold changes for genes across all brands. MutaMouse FE1 cells in culture (derived from lung epithelial cells) were exposed to cigarette smoke condensate (CSC) collected from 3 brands: Brand #1 M-bM-^@M-^S Full Flavor; Brand #3 M-bM-^@M-^S Regular; Brand #5 M-bM-^@M-^S Light King Size. Experiments were performed on 5 replicates per condition (i.e., n=5 per group); one replicate was removed from 4 groups later in the study. Cells were exposed at 70% confluence in 150 mm plates to either 45 M-BM-5g/ml or 90 M-BM-5g/ml CSC alongside cells exposed to 1% DMSO (Sigma-Alderich, Canada) in 1:1 DMEM:F12 (without FBS). Cells were exposed to CSC for 6 hours and then either: (a) immediately harvested, or (b) washed in PBS and cultured for another 4 hours in fresh media. The two time points were called 6 hours or 10 hours (6 hours exposure, 4 hours recovery for the latter). Cells were harvested with TRIzol (Invitrogen) and stored at -80oC. RNA was extracted and labelled, and hybridized to Agilent 22K mouse development microarrays following the manufacturer's protocol (Agilent Technologies Inc., USA). Arrays were washed and scanned on a ScanArray Express (Perkin-Elmer Life Sciences), and data were acquired with ImaGene 5.5 (BioDiscovery Inc.). Biological samples were hybridized in Cy5, and Stratagene Universal Reference RNA was hybridized in Cy3.
2012-04-01 | E-GEOD-30079 | biostudies-arrayexpress
Project description:Aspergillus fumigatus and Pseudomonas aeruginosa are the most prevalent fungal and bacterial pathogens, associated with cystic fibrosis-related infections, respectively. Although it is well established that P. aeruginosa eventually predominates as the primary pathogen, it is unknown why this is the case. Label-free quantitative proteomics was employed here to compare the cellular response to A. fumigatus, P. aeruginosa and sequential exposure to both pathogens in the type II alveolar epithelial cell line, A549, a model of the alveolar surface. In total, 2264 proteins were identified and the analysis of statistically significant (p<0.05; ±1.5 fold change), differentially abundant (SSDA) proteins, revealed an increase in the relative abundance of proteins associated with biological processes common to all pathogen-exposed groups. These included mitochondrial stress, energy metabolism and protein processing in the endoplasmic reticulum. Conversely, clear differences were observed between the cellular response to A. fumigatus or P. aeruginosa and following sequential exposure to both pathogens. The relative abundance of proteins associated with ribosomal activity appeared comparable between sequentially exposed cells and unexposed cells, but were substantially decreased in fungal- and bacterial-exposed cells. Furthermore, compared to unexposed cells, the relative abundance of proteins associated with the actin cytoskeleton, endocytosis, phagosome and lysosome were increased in A. fumigatus and P. aeruginosa-exposed cells, but appeared unchanged or decreased in sequentially exposed cells. This research provides novel insights into the whole cell proteomic response to A. fumigatus and P. aeruginosa, and highlights distinct differences following sequential exposure to both pathogens.
2019-11-11 | PXD014022 | Pride