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Direct exposure to SARS-CoV-2 and cigarette smoke increases infection severity and alters the stem cell-derived airway repair response

ABSTRACT: Direct exposure to SARS-CoV-2 and cigarette smoke increases infection severity and alters the stem cell-derived airway repair response

PROVIDER: PRJNA675538 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13010451.fastq.gz	Fastqsanger.gz
	SRR13010452.fastq.gz	Fastqsanger.gz
	SRR13010453.fastq.gz	Fastqsanger.gz
	SRR13010454.fastq.gz	Fastqsanger.gz

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Direct exposure to SARS-CoV-2 and cigarette smoke increases infection severity and alters the stem cell-derived airway repair response

Project description:To study the effect of cigarette smoke exposure on Sars-Cov2 infection, we directly exposed mucociliary air-liquid interface (ALI) cultures derived from primary human nonsmoker airway basal stem cells (ABSCs) to short term cigarette smoke and infected them with live SARS-CoV-2. We set out to examine the underlying mechanisms governing the increased susceptibility of cigarette smoke exposed ALI cultures to SARS-CoV-2 infection by usingle cell profiling of the cultures, which showed that interferon response genes were induced in SARS-CoV-2 infected airway epithelial cells in ALI cultures but smoking exposure together with SARS-CoV-2 infection reduced the interferon response.

2020-11-17 | GSE161089 | GEO

The reduction of dextran sulfate sodium-induced colitis severity in mice exposed to cigarette smoke is accompanied by specific gene pathway and microbial shifts.

Project description:Background and Aims: The impact of cigarette smoke on inflammatory bowel disease has been established by a large number of epidemiological, clinical, and preclinical studies. Exposure to cigarette smoke is associated with a higher risk of developing Crohn’s disease but is inversely correlated with the development, disease risks, progression, and relapse rate of ulcerative colitis. Few mechanistic studies have investigated the effect of cigarette smoke on intestinal inflammation and microbial composition. Methods: Three groups of mice were exposed to three different concentrations of cigarette smoke for a total of 4 weeks, including 5 days of dextran sulfate sodium treatment to induce colitis and a 7-day recovery period. A comprehensive and integrated comparative analysis of the global colon transcriptome and microbiome, as well as classical endpoints, was performed. Results: Cigarette smoke exposure significantly decreased the severity induced colitis. Colon transcriptome analysis revealed that cigarette smoke downregulated specific pathways in a concentration-dependent manner, affecting both the inflammatory state and composition of the gut microbiome. Metagenomics analysis demonstrated that cigarette smoke can modulate dextran sulfate sodium-induced dysbiosis of specific bacterial genera, contributing to resolve the inflammation or accelerate recovery. Conclusions: Cigarette smoke alters gut microbial composition and reduces inflammatory responses in a concentration-dependent manner. The present study lays the foundation for investigating potential molecular mechanisms responsible for the attenuation of colitis by cigarette smoke.

2020-03-03 | E-MTAB-7988 | biostudies-arrayexpress

NHBE exposed to cigarette smoke

Project description:normal human bronchial epithelial cultures from two cultures in parallel exposed to cigarette smoke (CS) or air (mock) at timepoints 4 hours and 24 hours. Keywords = cigarette smoke Keywords = microarray Keywords = bronchial cell Keywords = tobacco Keywords: time-course

2005-02-23 | GSE2302 | GEO

Kentucky assay: cigarette smoke

Project description:Kentucky assay: cigarette smoke

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Human airway epithelial responses to rhinovirus infection and cigarette smoke extract alone and in combination

Project description:This study was performed to test the hypothesis that cigarette smoke extract would alter the responses of primary cultures of human bronchial epithelial cells to infection with purified human rhinovirus 16. The data show marked alterations in rhinovirus-induced expression profiles of a number of genes in the presence of cigarette smoke extract (CSE).

2011-03-15 | GSE27973 | GEO

Modifications of the Rat Airway Explant Transcriptome by Cigarette Smoke

Project description:Although a number of animal model studies have addressed changes in gene expression in the parenchyma and their relationship to emphysema, much less is known about the pathogenesis of cigarette smoke-induced small airway remodeling. In this study, we exposed rat tracheal explants to whole smoke for 15 minutes, and then cultured the explants in air. The airway transcriptome was evaluated using RAE 230_2 GeneChips. By 2 hours after starting smoke exposure, expression levels of 502 genes were changed up or down by more than 1.5 times (p values <0.01 or less), and by 24 hours, 1870 genes were significantly changed up or down. These included genes involved in anti-oxidant protection, epithelial defense and remodeling, inflammatory mediators and transcription factors, and a number of unexpected genes including the MMP-12 inducer, tachykinin-1 (substance P). Pre-treatment of the explants with 1 x 10-7 M dexamethasone reduced the number of significantly changed genes by approximately 47% at 2 hr and 68% at 24 hours, and in almost all instances, reduced the magnitude of the smoke-induced changes. We conclude that even a very brief exposure to cigarette smoke can lead to rapid changes in the expression of a large number of genes in rat tracheal explants, and that these effects are directly mediated by smoke, without a need for exogenous inflammatory cells. Steroids, contrary to the usual belief, are able to ameliorate many of these changes, at least in this very acute model.

2009-06-01 | GSE15563 | GEO

Regional heterogeneity in response of airway epithelial cells to cigarette smoke

Project description:To investigate the biochemical and genetic alterations that occur in response to cigarette smoke exposure among airway epithelial cells from different sites in the lungs, we performed microarray-based analysis using small airway epithelial cells (SAEC) and normal human bronchial epithelial cells (NHBE) following 24 h of cigarette smoke extract (CSE). In microarray-based analysis, the small airway showed higher susceptibility to CS compared to the large airway, such as enhanced expression of inflammatory-related pathways including the TNF signaling pathway. Among the TNF-related genes, PTGS2, also known as COX-2, showed the greatest difference in expression levels, with higher CSE-induced increments of both mRNA and protein expression in SAEC compared to NHBE.

2018-01-16 | GSE107200 | GEO

Effect of cigarette smoke on gene expression in mammary epithelial cells [methylation]

Project description:Recent epidemiological studies demonstrate that both active and involuntary exposure to tobacco smoke increases the risk of breast cancer. Little is known, however, about the molecular mechanisms by which tobacco smoke contributes to breast carcinogenesis. To investigate these mechanisms we have analyzed gene expression and methylation in MCF 10A mammary epithelial cells chronically exposed to aqueous cigarette smoke extract (CSE).

2013-08-12 | GSE42623 | GEO

In Utero Cigarette Smoke Affects Allergic Airway Disease But Does Not Alter the Lung Methylome

Project description:Introduction: Prenatal and postnatal cigarette smoke exposure enhances the risk of developing asthma. Despite this as well as other smoking related risks, 11% of women still smoke during pregnancy. We hypothesized that cigarette smoke exposure during prenatal development generates long lasting differential methylation altering transcriptional activity that correlates with disease. Methods: In a house dust mite (HDM) model of allergic airway disease, we measured airway hyperresponsiveness (AHR) and airway inflammation between mice exposed prenatally to cigarette smoke (CS) or filtered air (FA). DNA methylation and gene expression were then measured in lung tissue. Results: We demonstrate that HDM-treated CS mice develop a more severe allergic airway disease compared to HDM-treated FA mice including increased AHR and airway inflammation. While DNA methylation changes between the two HDM-treated groups failed to reach genome-wide significance, 99 DMRs had an uncorrected p-value < 0.001. 6 of these 99 DMRs were selected for validation, based on the immune function of adjacent genes, and only 2 of the 6 DMRs confirmed the bisulfite sequencing data. Additionally, genes near these 6 DMRs (Lif, Il27ra, Tle4, Ptk7, Nfatc2, and Runx3) are differentially expressed between HDM-treated CS mice and HDM-treated FA mice. Conclusions: Our findings confirm that prenatal exposure to cigarette smoke is sufficient to modify allergic airway disease, however, it is unlikely that specific methylation changes account for the exposure-response relationship. These findings highlight the important role in utero cigarette smoke exposure plays in the development of allergic airway disease.

2015-11-19 | GSE71718 | GEO

Transcriptional response of Mycobacterium tuberculosis to cigarette smoke condensate

Project description:Mycbacterium tuberculosis was exposed to cigarette smoke condensate (CSC) in 7H9 dextrose culture media. The transcriptional response to cigarette smoke condensate was compared to that of exposure to the CSC diluent, DMSO..

2021-04-15 | GSE172041 | GEO

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