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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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). Cultured epithelial cells from each of 4 donors were exposed to medium alone, rhinovirus 16 (RV16) alone, CSE alone, or RV16 in the presence of CSE. After a 24 h incubation gene expression was assessed.

ORGANISM(S): Homo sapiens

SUBMITTER: David Proud

PROVIDER: E-GEOD-27973 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Cigarette smoke modulates expression of human rhinovirus-induced airway epithelial host defense genes.

Proud David D Hudy Magdalena H MH Wiehler Shahina S Zaheer Raza S RS Amin Minaa A MA Pelikan Jonathan B JB Tacon Claire E CE Tonsaker Tabitha O TO Walker Brandie L BL Kooi Cora C Traves Suzanne L SL Leigh Richard R

PloS one 20120712 7

Human rhinovirus (HRV) infections trigger acute exacerbations of chronic obstructive pulmonary disease (COPD) and asthma. The human airway epithelial cell is the primary site of HRV infection and responds to infection with altered expression of multiple genes, the products of which could regulate the outcome to infection. Cigarette smoking aggravates asthma symptoms, and is also the predominant risk factor for the development and progression of COPD. We, therefore, examined whether cigarette smo ...[more]

PMID: 22808255

Similar Datasets

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

Oxidative stress induces mitochondrial dysfunction and a protective unfolded protein response in RPE cells

Project description:How retinal pigmented epithelial (RPE) cells degenerate from oxidative stress in age-related macular degeneration (AMD) is incompletely understood. The study's intent was to identify key cytoprotective pathways activated by oxidative stress, and to determine the extent of their protection. Immunohistochemistry was used to identify the unfolded protein response (UPR) and mitochondria in the RPE of AMD samples. Maculas with early AMD had prominent IRE1α, but minimal mitochondrial TOM20 immunolabeling in mildly degenerated RPE. RPE cells treated with cigarette smoke extract (CSE), by microarray analysis, had over-represented genes involved in the antioxidant and unfolded protein response, and mitochondrial location. CSE induced the UPR sensors IRE1α, p-PERK, and ATP6, which activated CHOP. CHOP knockdown compromised cell viability after CSE exposure. At the same CSE doses, mitochondria generated superoxide anion and produced less ATP. In mice given intravitreal CSE, the RPE had increased IRE1α and decreased ATP, which elicited RPE epithelial-mesenchymal transition, as suggested by altered ZO1 immunolabeling of RPE flatmounts. Our experiments indicate that RPE cells exposed to oxidative stress respond with a cytoprotective antioxidant and unfolded protein response, but develop mitochondrial impairment that contributed to epithelial mesenchymal transition. With similar responses in the RPE of early AMD samples, these results suggest that mitochondria are vulnerable to oxidative stress while the ER elicits a protective response during early AMD. A total of 9 samples were analyzed: 3 control samples, 3 samples treated with 100ug/ml of Cigarette Smoke Condensate, and 3 samples treated with 250ug/ml of Cigarettes Smoke Condensate.

2014-01-30 | E-GEOD-49107 | biostudies-arrayexpress

Effect of radiation and cigarette smoke on breast cells

Project description:Exposure to genotoxic stresses such as cosmic radiation and second-hand tobacco smoke may increase the risk of breast cancer formation. Towards an understanding of how exposure to these genotoxic agents affect breast cancer biogenesis, we have shown that treating non-tumorigenic immortalized breast MCF 10A cells with low doses (0.1 Gray) of radiation as well as cigarette smoke condensate can generate a neoplastic breast cancer phenotype. The transformed phenotype promoted increased mammosphere numbers, altered cell cycle phases, and increased invasion and motility. In addition, exclusion of Hoechst 33342 dye, a surrogate marker for increased ABC transporters, was observed, which indicates a possible increase in drug resistance. Furthermore, differential gene expression profiles were generated from the individual and combination treatment. Overall, the results indicate that when normal breast cells are exposed to low dose radiation in combination with cigarette smoke condensate a phenotype is generated that exhibits traits indicative of neoplastic transformation. Taken together, these results provide a new insight into a possible etiology for breast cancer formation in individuals exposed to cosmic radiation and second-hand smoke. To study the effects of low dose ionizing radiation and tobacco smoke on breast cells, MCF 10A cells were treated either with radiation (Rad - 0.1 Gray) or cigarette smoke condensate (Csc - 10 microgram/ml of medium) or a combination of Rad + Csc). Following treatments, the cells were incubated for 72 hr, RNA extracted and analyzed for differential gene expression pattern.

2010-07-07 | E-GEOD-21066 | biostudies-arrayexpress

Mitochondrial mutations in cigarette smoke extract-chronically treated human oral OKF6 cells

Project description:The objective of this study was to analyze the mitochondrial mutations induced by chronic cigarette smoke extract treatment in human oral immortal OKF6 cells. The objective of this study was to analyze the mitochondrial mutations induced by chronic cigarette smoke extract treatment in human oral immortal OKF6 cells. 2 samples were included, a control passaged human oral immortal OKF6 cells and cigarette smoke extract-treated OKF6 cells. The chronic treatment for cigarette smoke extract is 7 months. Genomic DNAs were extracted from both cells and then used for Affymetix MitoChip Version 2.0 analysis.

2011-02-10 | E-GEOD-24414 | biostudies-arrayexpress

Organotypic human bronchial epithelial cultures (MucilAir) exposed to aqueous aerosol extracts of the 3R4F cigarette smoke and a novel tobacco product vapor

Project description:The current study was performed for analysis of the biological effects of vapor from novel tobacco vapor product in comparison with 3R4F cigarette smoke. This study was performed using a three-dimensional culture system composed of an air-liquid interface culture of primary normal human bronchial epithelial cells (MucilAir). The MucilAir tissues were subjected to 17 days of exposure to the aqueous extract of novel tobacco product vapor or 3R4F cigarette smoke. The number of differentially expressed genes increased in MucilAir tissues exposed to aqueous extract of each test product dependent on exposure duration. The number of differentially expressed genes was lower in the tissues exposed to aqueous extract of novel tobacco product vapor compared to the tissues exposed to aqueous extract of 3R4F cigarette smoke.

2020-04-15 | E-MTAB-8920 | biostudies-arrayexpress

Transcription profiling of rat tracheal airway explant treated with 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 gene chips. 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. Experiment Overall Design: 4x tracheal explants (approx 2-3ug) from each rat (n=6 rats) exposed to control (air), smoke (10 puffs of cigarette smoke, delivered during 15 mins), dexamethasone and dexamethasone + cigarette smoke were used for RNA extraction and hybridization on Rat230_2 Affymetrix microarrays. 1 rat, 4 explants and 4 condiditons. n= 6 rats per group/condition 12 animals = 48 samples total (47 went into analysis because 1 sample failing QC metrics)

2009-04-11 | E-GEOD-15563 | biostudies-arrayexpress

Gene expression data on lungs of wild-type and Rora (Retinoic acid related orphan receptor) mutant mice exposed to room air and smoke

Project description:Gene expression data on wild-type and Rora mutant mice exposed to room air and smoke. The results provide a general insight into the relationship of Rora to known DNA damage response pathways and its role in cigarette smoke-induced airspace enlargement. This dataset includes 4 wild-type mice exposed to room air, 4 wild-type mice exposed to cigarette smoke and 4 Rora mutant mice exposed to cigarette smoke.

2012-07-22 | E-GEOD-33512 | biostudies-arrayexpress

Expression data from adult mouse testis exposed to cigarette smoke in utero

Project description:In the context of male reproductive health, epidemiological studies have observed reduced testis size and abnormal sperm counts and morphology in adult men exposed in utero, although these findings are not always repeated. The ambiguity of these reports is confounded by a lack of controlled animal studies investigating the effects of maternal cigarette smoke exposure on male offspring reproductive health. In this study we examined the effects of cigarette induced reproductive toxicity on male offspring exposed during the gestational and weaning period using our novel direct nasal exposure mouse model of cigarette smoke-induced chronic obstructive pulmonary disease and female subfertility. This was done too gain a better understanding of the adverse effects of gestational maternal smoking on male offspring fertility. C57BL/6 5 week-old female mice were exposed via the nose-only to cigarette smoke [twelve 3R4F reference cigarettes (University of Kentucky, USA) twice/day, five times per week, for 12-18 weeks]. Each exposure lasted 60 minutes. Control mice received room air. In total, 27 mice underwent cigarette smoke exposure. Eleven week-old female mice exposed to cigarette smoke for 6 weeks were separated into groups of three and housed with a single control stud male aged 7-8 weeks with proven fertility for a maximum of 12 weeks. Females were monitored every second day for post-coital plugs and pregnancy. Pregnant females were separated into single cages and litter sizes/pup weights recorded. Smoke exposure via dams continued throughout mating/pregnancy/lactation until weaning of pups at 21days post birth. The testis of exposed offspring were then collected for RNA extraction and hybridization on an Illumina Sentrix Mouse ref-8 v2 Beadchip

2013-10-23 | E-GEOD-51530 | biostudies-arrayexpress

Repeated exposure and switching study of cigarette smoke and next generation tobacco product using 3D human bronchial epithelial cells

Project description:Next generation product such as heat-not-burn type product and e-cigarette emit lower yields of chemical constituents than cigarette because combustion of tobacco leaves is not associated with their vapor generation. Therefore it is expected that the usage of these product bring beneficial impact on public health. However, risk-reduced potential as well as risk concerns in long-term use of these products has not yet been fully understood. In this study, we intended to estimate the risk reduced potential of our proprietary novel tobacco vapor product (NTV) by repeated exposure of in vitro 3D bronchial epithelial cells to NTV vapor in comparison with repeated exposure to cigarette smoke. In addition, to reflect the realistic situation of smokers, exposure switching from cigarette smoke to NTV vapor and cigarette smoke exposure cessation were conducted.

2020-03-31 | E-MTAB-8155 | biostudies-arrayexpress

Human primary alveolar epithelial cells (hAEC) exposed to cigarette smoke extract

Project description:hAEC cells were exposed to cigarette smoke extract (CSE) or PBS for 48h, and gene expression was evaluated by RNA-seq.In this study we explored the effect of cigarette smoke on the gene expression profile.

2021-10-28 | GSE186359 | GEO

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