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Electronic cigarette exposure disrupts blood-brain barrier integrity, promotes neuroinflammation, and leads to cognitive dysfunction

ABSTRACT: Electronic cigarette exposure disrupts blood-brain barrier integrity, promotes neuroinflammation, and leads to cognitive dysfunction

PROVIDER: PRJNA596914 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10744457.fastq.gz	Fastqsanger.gz
	SRR10744458.fastq.gz	Fastqsanger.gz
	SRR10744459.fastq.gz	Fastqsanger.gz
	SRR10744460.fastq.gz	Fastqsanger.gz
	SRR10744461.fastq.gz	Fastqsanger.gz

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Similar Datasets

Electronic cigarette exposure disrupts blood-brain barrier integrity, promotes neuroinflammation, and leads to cognitive dysfunction

Project description:Electronic cigarette (EC) use has grown substantially since entry into the US market, particularly among adolescents and combustible tobacco users. Despite growing popularity and claims of harm reduction, the health effects of these products outside the lung is poorly understood. Several constituents of cigarette smoke (CS) with known neurovascular and inflammatory effects are present in EC liquids or formed during the generation of vapor. The present study characterizes the impact of EC exposure on neuroinflammation and blood-brain barrier (BBB) function, and provides comparison of outcomes with reference cigarette exposure normalized to comparable levels of nicotine delivery. Additionally, the contribution of nicotine to observed effects is elucidated through comparison with EC liquids which are verified to be nicotine-free. C57BL/6 mice are exposed to 2 hrs of daily EC vapor or CS, beginning at 8 wks of age. Changes in BBB gene expression are first characterized by whole exome sequencing of isolated brain microvessels following chronic (2 month) EC exposure.

2020-11-23 | GSE142400 | GEO

Molecular impact of electronic cigarette aerosol exposure in human bronchial epithelium

Project description:Analysis of primary human bronchial epithelial cells grown in air liquid interface, exposed in vitro to whole tobacco cigarette smoke (48 puffs, 48 minutes) and electronic cigarette aerosol (400 puffs, 200 minutes). Electronic cigarette exposures included two flavors (menthol, tobacco) both with, and without nicotine.

2016-10-12 | GSE82137 | GEO

Electronic cigarette exposure disrupts blood-brain barrier integrity and promotes neuroinflammation.

Project description:Electronic cigarette (e-cigarette) use has grown substantially since inception, particularly among adolescents and combustible tobacco users. Several cigarette smoke constituents with known neurovascular effect are present in e-cigarette liquids or formed during the vapor generation. The present study establishes inhaled models of cigarette and e-cigarette use with normalized nicotine delivery, then characterizes the impact on blood-brain barrier (BBB) function. Sequencing of microvessel RNA following exposure revealed downregulation of several genes with critical roles in BBB function. Reduced protein expression of Occludin and Glut1 is also observed at the tight junction in all groups following exposure. Pro-inflammatory changes in leukocyte-endothelial cell interaction are also noted, and mice exposed to nicotine-free e-cigarettes have impaired novel object recognition performance. On this basis, it is concluded that long term e-cigarette use may adversely impact neurovascular health. The observed effects are noted to be partly independent of nicotine content and nicotine may even serve to moderate the effects of non-nicotinic components on the blood-brain barrier.

| S-EPMC7899242 | biostudies-literature

Abnormal expression profile of plasma exosomal microRNAs in exclusive electronic cigarette adult users

Project description:Exposure to electronic cigarette (e-cigarette) aerosol has been linked to a number of health concerns, including DNA damage, elevated oxidative stress, release of inflammatory cytokine, and dysfunctions in epithelial barriers. However, little is known about the effect of exclusive e-cigarette use on expression profiles of exosomal miRNAs, which play critical regulatory roles in many inflammatory responses and disease process including cancer. We aim to compare the exosomal microRNAs expression profile between exclusive e-cigarette users and normal controls without any tobacco product use (non-users). Using blood and urine samples from exclusive e-cigarette users and non-users in the Population Assessment of Tobacco and Health (PATH) Wave 1 study (2013-2014), we examined exosomal microRNAs expression levels through Illumina NextSeq 500/550 sequencing. We identified microRNAs that have significantly higher expression levels in exclusive e-cigarette users than non-users. Gene enrichment analysis of these significant exosomal microRNAs showed their involvement in cancer related pathways, which might indicate a potential elevated risk of cancer among exclusive e-cigarette users.

2024-07-10 | GSE253603 | GEO

Gene Expression Alterations in Bronchial Epithelium of Electronic Cigarette Users

Project description:Background: While electronic cigarette (ECIG) use is rapidly rising, their safety profile remains uncertain. The effects of tobacco cigarette (TCIG) smoke on bronchial airway epithelial gene-expression have provided insights into tobacco-related disease pathogenesis. Understanding the impact of electronic cigarettes (ECIGs) on airway gene-expression could provide insights into their potential long-term health effects. Objectives: We sought to compare the bronchial airway gene-expression profiles of former TCIG smokers now using ECIGs with the profiles of former and current TCIG smokers. Methods: We performed gene-expression profiling of bronchial epithelial cells collected from TCIG smokers not using ECIGs (n=21), former smokers using ECIGs (n=15), and current TCIG smokers not using ECIGs (n=9). We then compared our findings with previous studies of the effects of TCIG use on bronchial epithelium, as well an in vitro model of ECIG exposure. Results: Amongst 3,165 genes whose expression varied between the three study groups (q < 0.05), we identified 468 genes significantly altered in ECIG users relative to former smokers (p < 0.05). 79 of these genes were up or down-regulated concordantly between ECIG and TCIG. We did not detect ECIG-associated gene expression changes in known pathways associated with TCIG usage. Genes downregulated in ECIG users are enriched among the genes most downregulated by exposure of airway epithelium to ECIG vapor in vitro. Conclusions: TCIG exposure was associated with a larger number of airway gene-expression changes than with ECIG exposures. ECIGs induce both distinct and shared patterns of gene expression relative to TCIGs in the bronchial airway epithelium.

2019-10-09 | GSE112073 | GEO

Gene Expression Alterations in Bronchial Epithelium of Electronic Cigarette Users

Project description:Gene Expression Alterations in Bronchial Epithelium of Electronic Cigarette Users

| PRJNA439243 | ENA

Saliva and Lung Microbiome Associations With Electronic Cigarette Use and Smoking

Project description:Saliva and Lung Microbiome Associations With Electronic Cigarette Use and Smoking

| PRJNA749564 | ENA

Gene Expression Changes from E-Cigarette Exposure During Early Pregnancy

Project description:Electronic nicotine delivery system (E-Cigarette) use is prevalent among pregnant women. We examined whether E-Cigarette exposure impairs implantation. RNA microarray was performed on day 4.5 pseudopregnant mice exposed to E-Cigarettes or sham during each day of pregnancy.

2019-09-12 | GSE131077 | GEO

Transcriptome characterization of human gingival mesenchymal and periodontal ligament stem cells in response to Electronic-cigarette

Project description:The change of transcriptome and related biological functions affected by tobacco smoke and Electronic-cigarette (E-cig) to human gingival mesenchymal (GMSC) and periodontal ligament stem cells (PDLSCs) are not fully understood. Here, we collected GMSCs and PDLSCs from systemically healthy patients due to the premolars and extracted for orthodontic reasons, and treated with tobacco smoke (G1, P1), E-cig smoke with original flavor (G2, P2), E-cig smoke with menthol flavor (G3, P3), E-cig liquid with original flavor (G4, P4), and E-cig liquid with menthol flavor (G5, P5) by the optimal conditions of LC50, and conducted RNA-seq to compare with untreated control (G0, P0).

2022-06-17 | E-MTAB-11797 | biostudies-arrayexpress

Electronic cigarettes

Project description:Electronic cigarettes (e-cigarettes) have gained their popularity as a substitute for cigarettes or cigars. Despite the widespread use of flavoring chemicals in e-cigarettes, the health impacts of the flavoring compounds, in particular their effects on critical cellular function in the lung, remain largely unknown. The goal of this study was to identify transcriptomic changes and impacted biological pathways in primary human bronchial epithelial cells (HBECs) exposed to flavoring chemicals (diacetyl or 2,3-pentanedione) and to flavored e-cigarette smoke. An airway-liquid interface culturing method was used to differentiate primary human bronchial epithelial cells (HBECs) into mature epithelial cells, which were then treated with 25 ppm diacetyl, 100 ppm 2,3 pentanedione, or e-cigarette smoke solution containing 2 ppm diacetyl. Poly(A)-selected RNA-Seq libraries were prepared with the PrepX RNA-Seq for Illumina Library kit. An Illumina HiSeq 2500 instrument was used to generate 50 base pair single-end reads. STAR was used to align sequencing reads to the hg38 reference genome, and HTSeq was used to quantify transcript levels. DESeq2 was used to perform differential expression analysis.

2019-08-21 | GSE118431 | GEO

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