Electronic vaping preferentially target respiratory bronchioles leading to severe bronchiolitis in experimentally-exposed macaques
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ABSTRACT:
PROVIDER: PRJNA818290 | ENA |
REPOSITORIES: ENA
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Project description:Electronic cigarette use has increased dramatically over the past three years, despite numerous reports of acute lung injury and even death. In this report we provide evidence from a nonhuman primate model for Electronic Vapor-Induced Lung Injury (EVALI), demonstrating significant lung pathology from electronic vaping (EV). Here we characterized the particle size and pathogenic effects induced by EV exposure of nonhuman primates using the commercial nicotine JUUL® pod modular devices. Vaping aerosols appear to preferentially and exclusively target the bronchioles while bypassing larger bronchi. We demonstrate a significantly smaller particle size, generated by the EV device relative to combustion product aerosols produced by conventional cigarettes. Histopathologically, vaping aerosols appear to preferentially and exclusively target the bronchioles while bypassing larger bronchi which is consistent with a significanlty smaller particle size compared to cigarette smoke. Our immunohistochemical and RNAseq studies provide further evidence for severe small airway inflammation and dysregulation of gene expression within immune cells derived from bronchial lavage, respectively. Our findings raise major concerns regarding the safety of e-cigarettes, and provide a mechanism for the preferential induction of lung injury by EV. Our results, in a species whose lung architecture is the closest possible approximation of that of a human adolescent, suggest the danger of the EV device itself and resultant small particulate aerosols produced, preferentially entering and damaging a highly susceptible part of the respiratory system.
2022-07-01 | GSE199072 | GEO
Project description:Acute viral bronchiolitis (NMS)
| PRJNA450429 | ENA
Project description:Acute viral bronchiolitis (PBMC)
| PRJNA450430 | ENA
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
Project description:electronic Medical Records & Genomics (eMERGE)
| PRJNA158491 | ENA
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
Project description:Human respiratory syncytial virus (HRSV) is the main cause of bronchiolitis during the first year of life, but other viruses such as rhinovirus also occur and are clinically indistinguishable. In hospitalized infants with bronchiolitis, the analysis of the peripheral blood mononuclear cells (PBMC) gene expression might be useful for identification the etiologies caused by HRSV and human rhinovirus (HRV) and to the development of future tests, as well as to elucidate the pathogenic mechanisms triggered by different viral agents and new therapeutic possibilities. In this study, we conducted a comparative global gene expression analysis of infants with acute viral bronchiolitis infected by HRSV (HRSV group) or HRV (HRV group).
2019-03-19 | GSE124124 | GEO
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