Revealing oral microbiota composition and functionality associated with heavy cigarette smoking
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB53577 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR9850640.fastq.gz | Fastqsanger.gz | |||
| ERR9850650.fastq.gz | Fastqsanger.gz | |||
| ERR9850660.fastq.gz | Fastqsanger.gz | |||
| ERR9850670.fastq.gz | Fastqsanger.gz | |||
| ERR9850680.fastq.gz | Fastqsanger.gz |
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Project description:BACKGROUND:Heavy tobacco smoking, a hallmark feature of lung cancer, is drastically predominant in Middle Eastern populations. The precise links between nicotine dependence and the functional contribution of the oral microbiota remain unknown in these populations. METHODS:We evaluated the composition and functional capabilities of oral microbiota with relation to cigarette smoking in 105 adults through shotgun metagenomics using buccal swabs. RESULTS:The oral microbiota composition in our study subjects was dominated by the phyla Firmicutes, Proteobacteria, Actinobacteria, and Bacteroidetes, in addition to the genera Prevotella and Veillonella, similar to previously described westernized cohorts. Furthermore, the smoker's oral microbiota represented a significant abundance of Veillonella dispar, Leptotrichia spp. and Prevotella pleuritidis when compared to non-smokers. Within the smoking groups, differential relative abundance testing unveiled relative abundance of Streptobacillus hongkongensis, Fusobacterium massiliense, Prevotella bivia in high nicotine dependent compared to low nicotine dependent profiles based on Fagerström Test for Nicotine Dependence. Functional profiling showed marked differences between smokers and non-smokers. Smokers exhibited an enrichment of Tricarballylate utilization and Lactate racemization when compared to the non-smokers. According to their nicotine dependence, enrichment of Xanthosine utilization, p-Aminobenzoyl-Glutamate utilization, and multidrug efflux pump in Campylobacter jejuni biosynthesis modules were detected in the high nicotine dependent group. CONCLUSIONS:These compositional and functional differences may provide critical insight on how variations in the oral microbiota could predispose to respiratory illnesses and smoke cessation relapse in cigarette smokers. In particular, the observed enrichment of Fusobacterium and Prevotella in the oral microbiota possibly suggests an intriguing linkage to gut and lung cancers.
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Project description:In our previous study, we identified global genetic and epigenetic aberrations in the tumors of oral squamous cell carcinoma (OSCC) patients who were habitual smokers. We hypothesized that cigarette smoke might play a role in oral malignant transformation. DOK cell line is a dysplasitc oral keratinocyte derived from a heavy smoker with OSCC. The differentially expressed genes between DOK and normal human oral keratinocytes (HOK) may provide important information about OSCC carcinogenesis mediated by cigarette smoking.
2015-12-31 | GSE54861 | GEO
Project description:In our previous study, we identified global genetic and epigenetic aberrations in the tumors of oral squamous cell carcinoma (OSCC) patients who were habitual smokers. We hypothesized that cigarette smoke might play a role in oral malignant transformation. DOK cell line is a dysplasitc oral keratinocyte derived from a heavy smoker with OSCC. The differentially expressed genes between DOK and normal human oral keratinocytes (HOK) may provide important information about OSCC carcinogenesis mediated by cigarette smoking. Total RNA was collected from DOK and HOK cells followed by gene expression microarray analysis.
2015-12-31 | E-GEOD-54861 | biostudies-arrayexpress
Project description:Alveolar macrophages from never smokers and active smokers were isolated by bronchoalveolar lavage and gene expression was measured. Chronic cigarette smoke exposure, as occurs in smoker's lungs, leads to significant changes in gene expression. Of note, RNA was isolated immediately following bronchoscopy. Alveolar macrophage levels were >95%.
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Project description:Cigarette smoke components have a proven negative influence on human health. Adverse metabolic effects have been observed in tissues and single cells. As T-lymphocytes get in contact with affected organs (e.g. lung) or cells (e.g.erythrocytes), as well as with smoke components and bioactive molecules, whose production is influenced by them, we compared the gene exression profiles in these cells of the adaptive immune system of three male heavy smokers and three male non-smokers We combined rapid immuno-precipitation and Affymetrix GeneChip® HG U133A2.0 microarray analysis to analyse the data set. 88 genes were found significantly (T-test) differentially expressed by a factor of 1.5-fold or larger between smokers and non-smokers. Using the gene function groups of the gene ontology consortium to categorize the functions of the differentially expressed genes the group termed “response to stimulus” was found most significantly affected by smoking. Our data indicate a prominent role of cytotoxic T-lymphocytes in response to smoking. Several genes that are typically found in these cells are found regulated although the ratio of cytotoxic and helper T-lymphocytes remained unchanged in smokers. Keywords: gene expression changes in T-lymphocytes in response to smoking
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Project description:Transcriptomic analysis of the effects of cigarette smoking on the gene expression in blood in humans Analysis of gene expression in blood from 22 smokers and 22 non-smokers
2012-10-01 | E-GEOD-23323 | biostudies-arrayexpress
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Project description:Although smoking-induced lung disease tends to be more common in the upper lobe, it is not known if this results from the skewed distribution of inhaled cigarette smoke or increased susceptibility of the upper lobes to these disorders. The distribution of inhaled cigarette smoke within the lung is complex, depending on lung pressure-volume relationships, gravity, individual smoking habits and the properties of the individual components of cigarette smoke. With the knowledge that the small airway epithelium is the earliest site of smoking-induced lung disease, and that the small airway epithelium is acutely sensitive to inhaled cigarette smoke with significant changes in the up- and down-regulation of hundreds of genes, we compared upper vs lower lobe gene expression in the small airway epithelium of the same cigarette smokers to determine if the gene expression patterns were similar or different. Active smokers (n=11) with early evidence of smoking-induced lung disease (normal spirometry but low diffusing capacity) underwent bronchoscopy and brushing of the small airway epithelium to compare upper vs lower lobe genome-wide gene expression assessed by microarray. Interestingly, cluster and principal component analysis demonstrated that, for each individual, the expression of the known small airway epithelium smoking-responsive genes were remarkably similar as upper vs lower lobe pairs, although, as expected, there were differences in the smoking-induced changes in gene expression from individual to individual. Thus, while there may be topographic differences in the distribution of cigarette smoke, sufficient smoke reaches the upper vs lower lobe small airway epithelium so that, within each smoker, the upper vs lower lobe gene expression are similar. These observations support the concept that the topographic differences in the occurrence of the smoking-induced lung diseases are likely secondary to topographic differences in the susceptibility of the upper vs lower lobes to cigarette smoke, not the topographic differences in distribution of inhaled cigarette smoke.
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Project description:There are inherited genetic factors that cause different responses to cigarette smoking exposure among individuals. We tried to identify these differences in heavy smokers by examining copy number variations (CNVs) between lung cancer patients and healthy controls. To rule out the CNVs infulenced by age, smoking history and sex, those were matched in both groups.
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