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Induction of the IL-6/signal transducer and activator of transcription pathway in the lungs of mice exposed to tobacco

ABSTRACT: We have examined the impact of subchronic levels of tobacoo smoke on murine lungs. We have used high density DNA microarray and analysed lung tissues from mice exposed to mainstream tobacco smoke (MTS). Our results reveal induction of inflammatory cytokine interleukin-6 (IL-6) and its antagonist suppressor of cytokine signalling (SOCS3) mRNA in smoking group. We also show that these changes are transient and are reversed completely after a period of cessation of smoking. Keywords: Toxicology, disease state analysis, biomarkers of health effects

ORGANISM(S): Mus musculus

PROVIDER: GSE12930 | GEO | 2009/09/14

SECONDARY ACCESSION(S): PRJNA110851

REPOSITORIES: GEO

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Transcription profiling of mouse lung tissue after exposure to mainstream tobacco smoke

Project description:We have examined the impact of subchronic levels of tobacoo smoke on murine lungs. We have used high density DNA microarray and analysed lung tissues from mice exposed to mainstream tobacco smoke (MTS). Our results reveal induction of inflammatory cytokine interleukin-6 (IL-6) and its antagonist suppressor of cytokine signalling (SOCS3) mRNA in smoking group. We also show that these changes are transient and are reversed completely after a period of cessation of smoking. Experiment Overall Design: Male C57B1/CBA mice were exposed to MTS from two cigarettes daily, 5 days/week for 6 or 12 weeks. Mice were sacrificed immediately, or six weeks following the last cigarette. Left lung lobes were removed and flash frozen. Total RNA was isolated from a small part of the frozen lung and was hybridized against universal mouse reference RNA to Agilent Oligo DNA microarrays (Agilent Technologies) containing 22,000 transcripts. Microarrays were normalized using a global LOWESS approach and analyzed by MAANOVA 2.0 and SAM. Microarray results were validated by real time RT-PCR. Impact of alteration in expression of select genes was further validated by analysing their total protein levels in lung tissue homogenates.

2009-09-18 | E-GEOD-12930 | biostudies-arrayexpress

Structural, Functional and Molecular Impact on the Cardiovascular System in ApoE-/- Mice Exposed to Aerosol from modified risk tobacco products, the Carbon Heated Tobacco Product 1.2 and the Tobacco Heating System 2.2 compared to Cigarette Smoke effects (miRNA data).

Project description:AIM: To investigate the molecular, structural, and functional impact of aerosols from two heat-not-burn-based MRTPs, the Carbon Heated Tobacco Product (CHTP) 1.2 and Tobacco Heating System (THS) 2.2, compared with that of cigarette mainstream smoke (CS) on the cardiovascular system of ApoE-/- mice. METHOD: Female ApoE-/- mice were exposed to aerosols from THS 2.2 and CHTP 1.2 or to CS from 3R4F for up to 6 months at matching nicotine concentrations. A cessation and a switching group (3 months exposure to 3R4F CS followed by filtered air or CHTP 1.2 for 3 months) were included. Cardiovascular effects were investigated using echocardiography, histopathology, immunohistochemistry, and transcriptomics. RESULTS: Continuous exposure to aerosols from CHTP 1.2 and THS 2.2 did not affect the atherosclerosis progression, heart function, left ventricular structure and cardiovascular transcriptome. Exposure to CS from 3R4F triggered atherosclerosis progression, reduced systolic ejection fraction and fractional shortening, caused heart left ventricle hypertrophy and initiated significant dysregulation in the transcriptomes of the heart ventricle and thoracic aorta. Importantly, smoking cessation and switching to CHTP 1.2 aerosol similarly improved the structural, functional, and molecular changes caused by 3R4F CS. CONCLUSION: Exposure to aerosols from CHTP 1.2 and THS 2.2 lacked most of the CS exposure-related functional, structural and molecular effects. Smoking cessation or switching to CHTP 1.2 aerosol caused a similar recovery from the 3R4F CS effect in the ApoE-/- model with no further acceleration of plaque progression beyond the aging-related rate.

2021-08-16 | E-MTAB-7981 | biostudies-arrayexpress

2021-08-16 | E-MTAB-7980 | biostudies-arrayexpress

Transcription profiling of mouse heart tissue from animals exposed to mainstream tobacco smoke

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Effect of cessation after initial exposure to cigarette smoke

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2013-10-19 | E-MTAB-1390 | biostudies-arrayexpress

A global toxicogenomic analysis investigating the mechanistic differences between tobacco and marijuana smoke condensates in vitro

Project description:Like tobacco smoking, habitual marijuana smoking causes numerous adverse pulmonary effects. However, the mechanisms of action involved, especially as compared to tobacco smoke, are still unclear. To uncover putative modes of action, this study employed a toxicogenomics approach to compare the toxicological pathways perturbed following exposure to marijuana and tobacco smoke condensate in vitro. Condensates of mainstream smoke from hand-rolled tobacco and marijuana cigarettes were similarly prepared using identical smoking conditions. Murine lung epithelial cells were exposed to low, medium and high concentrations of the smoke condensates for 6 hr. RNA was extracted immediately or after a 4-hr recovery period and hybridized to mouse whole genome microarrays. Tobacco smoke condensate (TSC) exposure was associated with changes in xenobiotic metabolism, oxidative stress, inflammation, and DNA damage response. These same pathways were also significantly affected following marijuana smoke condensate (MSC) exposure. Although the effects of the condensates were largely similar, dose-response analysis indicates that the MSC is substantially more potent than TSC. In addition, steroid biosynthesis, apoptosis, and inflammation pathways were more significantly affected following MSC exposure, whereas m-phase cell cycle pathways were more significantly affected following TSC exposure. MSC exposure also appeared to elicit more severe oxidative stress than TSC exposure, which may account for the greater cytotoxicity of MSC. This study shows that in general, MSC impacts many of the same molecular processes as TSC. However, subtle pathway differences can provide insight into the differential toxicities of the two complex mixtures.

2014-02-06 | GSE44603 | GEO

Transcriptomics-based characterization of smoking and cessation effects in mouse muscle

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2012-09-01 | E-GEOD-18033 | biostudies-arrayexpress

Project description:RNA was obtained longitudinally from normal nasal epithelium of smokers who have quit smoking over 6 months period. Statistical analysis of gene expression data identified genes differentially expressed with short-term smoking cessation and categorized the kinetics of of these genes in different biological functions with different dynamics following smoking cessation.

2019-05-15 | GSE83364 | GEO

The impact of long term cigarette smoke, but not Tobacco Heating System 2.2 exposure on the genes involved in cardiac muscle structure and function in Apoe-/- mouse.

Project description:Cigarette smoking is a major risk factor for the development and progression of diseases such as cardiovascular disease (CVD) and chronic obstructive pulmonary disease (COPD). Modified risk tobacco products (MRTP) are designed to reduce smoking-related health risks. Suitable animal models are important for understanding smoke-induced pathogenesis. Over an 8-month period, hallmarks of CVD were investigated in ApoE?/? mice exposed to conventional cigarette smoke (CS) or to an aerosol from a candidate RRP, the tobacco heating system (THS2.2). In addition to chronic exposure, cessation or switching to THS2.2 after 2 months of CS were investigated.ﾠ The aim of this study was to evaluate the transcriptomics response of mouse heart tissue after exposure to 3R4F and a potential reduced risk tobacco product, Tobacco Heating System 2.2 (THS2.2). The transcriptomic analysis of heart tissue, showed that cigarette smoke strongly impacted the differential expression of genes at long term of smoke exposure at 6 and 8 month, whereas the new THS2.2 not burning product donﾒt present any significant impact on the genes expression on cardiovascular tissue. In a similar manner, cessation and switching exposure donﾒt present any significant regulation of genes. Functional analysis of differentially expressed genes shown that 3R4F exposure strongly regulate the cytoskeleton organization and contraction and shown a down regulation of actin, actinin alpha 4, the main component of sarcomere structure. These preliminary results suggest that the conventional smoking product may favours the development of cardiomyopathy via a direct impact of the cardiomyocytes structure and that the inflammatory process could also be affected by the smoke exposure and could be responsible for the non-adaptive response of heart to a stress.

2017-02-27 | E-MTAB-3900 | biostudies-arrayexpress

Lung gene expression of ApoE-/- mice in an 8-month inhalation study to assess exposure effects for a candidate modified risk tobacco product, THS 2.2 compared with conventional cigarettes

Project description:Cigarette smoking is a major risk factor for the development and progression of diseases such as cardiovascular disease (CVD) and chronic obstructive pulmonary disease (COPD). Modified risk tobacco products (MRTP) are designed to reduce smoking-related health risks. Suitable animal models are important for understanding smoke-induced pathogenesis. Over an 8-month period, hallmarks of both COPD and CVD were investigated in ApoE?/? mice exposed to conventional cigarette smoke (CS) or to an aerosol from a candidate MRTP, the tobacco heating system (THS2.2). In addition to chronic exposure, cessation or switching to THS2.2 after 2 months of CS were investigated.ﾠ In a systems toxicology approach, classical end points (e.g., physiology, histology) were complemented with transcriptomics, lipidomics, and proteomics analyses. CS induced nasal epithelial hyperplasia and metaplasia, lung inflammation, and emphysematous changes (impaired pulmonary function, alveolar damage). Atherogenic effects of CS exposure were altered lipid profiles and increased aortic plaque formation. Exposure to THS2.2 aerosol (nicotine concentration matched to CS ﾖ 29.9 mg/m3) did not induce lung inflammation and emphysema, nor did it consistently change the lipid profile or enhance the plaque area. Cessation and switching caused reversal of inflammatory responses and no progression of initial emphysematous changes and aortic plaque area. Biological processes, e.g., senescence, inflammation, proliferation, were significantly impacted in 3R4F-exposed, but not in THS2.2-exposed tissues. Cessation or switching reduced these perturbations to become nearly indistinguishable from sham-exposure. In conclusion, the mouse model indicated retarded progression of atherosclerotic and emphysematous changes upon cessation or switching to THS2.2 which alone had no adverse effects.

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