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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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COPD progression in c57bl/6 mice

ABSTRACT: Smoking of combustible cigarettes has a major impact on human health, so the tobacco industry is developing modified risk tobacco products (MRTP) to reduce this health risk. Using a systems toxicology approach in a model of chronic obstructive pulmonary disease (C57BL/6 mice), we assessed the potential of such a prototype (pMRTP) to reduce health risk. We investigated physiological endpoints in parallel with transcriptomics, lipidomics, and proteomics profiles in mice exposed to conventional cigarette smoke (3R4F) or a pMRTP aerosol for up to 7 months. We also included a cessation group and a switching-to-pMRTP group (after 2 months of 3R4F exposure) in addition to the control (fresh air-exposed) group, to understand the potential risk reduction of switching to pMRTP compared with continuous 3R4F exposure. The present manuscript describes the study design, setup, and implementation, as well as the generation, processing, and quality control analysis of the toxicology and "omics" datasets that are accessible in public repositories for further studies.

ORGANISM(S): Mus musculus

SUBMITTER: Sam Ansari

PROVIDER: E-MTAB-3150 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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COPD progression in C57l/6 mice in response to chronic exposure (up to 7 months) to conventional cigarette smoke or a prototype modified risk tobacco product (pMRTP) and the impact of cessation or switching to pMRTP after initial exposure to conventional cigarette smoke

Project description:Smoking of combustible cigarettes has a major impact on human health, so the tobacco industry is developing modified risk tobacco products (MRTP) to reduce this health risk. Using a systems toxicology approach in a model of chronic obstructive pulmonary disease (C57BL/6 mice), we assessed the potential of such a prototype (pMRTP) to reduce health risk. We investigated physiological endpoints in parallel with transcriptomics, lipidomics, and proteomics profiles in mice exposed to conventional cigarette smoke (3R4F) or a pMRTP aerosol for up to 7 months. We also included a cessation group and a switching-to-pMRTP group (after 2 months of 3R4F exposure) in addition to the control (fresh air-exposed) group, to understand the potential risk reduction of switching to pMRTP compared with continuous 3R4F exposure. The present manuscript describes the study design, setup, and implementation, as well as the generation, processing, and quality control analysis of the toxicology and 'omics' datasets that are accessible in public repositories for further studies.

2017-08-05 | E-MTAB-5281 | biostudies-arrayexpress

Comprehensive systems biology analysis of a seven-month cigarette smoke inhalation study in C57BL/6 mice.

Project description:Combustible cigarette smoking has major impact on human health. In order to reduce smoking-related health risk, the tobacco industry is developing modified risk tobacco products (MRTP). To assess the potential of such a prototype (pMRTP) to reduce health risk, we used C57BL/6 mice, model of chronic obstructive pulmonary disease (COPD), in a systems toxicology approach to investigate in a large, controlled study, classical toxicology end points in parallel to transcriptomics, lipidomics, and proteomics profiles in mice exposed to conventional cigarette smoke (3R4F) or a pMRTP aerosol for up to 7 months. We also included a cessation group and a switching-to-pMRTP group (after 2 months of 3R4F exposure), in addition to the control (fresh air exposed) group, to understand the potential benefit of switching to pMRTP for smokers who cannot or do not want to quit smoking. For quantitative proteomics analysis with the iTRAQ method, lung tissue samples from six mice (ie, six biological replicates) were analyzed for each exposure condition and time point (months 1, 3, 5, and 7 for 3R4F and pMRTP exposure and months 3, 5, and 7 for cessation and switch).

2016-01-04 | PXD001369 | Pride

Comprehensive systems biology analysis of a seven-month cigarette smoke inhalation study in C57BL/6 mice

Project description:Smoking of combustible cigarettes has a major impact on human health. Using a systems toxicology approach in a model of chronic obstructive pulmonary disease (C57BL/6 mice), we assessed the health consequences in mice of smoke derived from a prototype modified risk tobacco product (pMRTP) as compared to conventional cigarettes. We investigated physiological and histological endpoints in parallel with transcriptomics, lipidomics, and proteomics profiles in mice exposed to a reference cigarette (3R4F) smoke or a pMRTP aerosol for up to 7 months. We also included a cessation group and a switching-to-pMRTP group (after 2 months of 3R4F exposure) in addition to the control (fresh air-exposed) group, to understand the potential risk reduction of switching to pMRTP compared with continuous 3R4F exposure and cessation. </p> The dataset shared here describes the lipidomics analyses performed on lung, liver, and plasma of these mice at multiple time points. Lipids were characterized using, in addition to (untargeted) shotgun lipidomics, a set of targeted methods to specifically characterize sphingolipids, ceramides, triglycerides, eicosanoids, and gangliosides.

2015-11-19 | MTBLS143 | MetaboLights

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.

2015-12-01 | E-MTAB-3681 | biostudies-arrayexpress

Systems toxicology assessment of CHTP1.2 [RNE Data]

Project description:Modified risk tobacco products (MRTPs) have the potential to reduce smoking-related health risks. The Carbon Heated Tobacco Product 1.2 (CHTP1.2) is a potential MRTP that uses a pressed carbon heat source to generate an aerosol by heating tobacco. This study reports the results from the systems toxicology arm of a 90-day rat inhalation study (OECD test guideline 413) to assess the effects of CHTP1.2 aerosol compared with cigarette smoke (CS). Rats were exposed to filtered air (sham), to CHTP1.2 aerosol (at 15, 23 and 50 µg nicotine / L), or to the 3R4F reference cigarette smoke (at 23 µg nicotine / L).

2018-04-10 | E-MTAB-6320 | biostudies-arrayexpress

Systems toxicology assessment of CHTP1.2 [Liver Data]

2018-04-10 | E-MTAB-6317 | biostudies-arrayexpress

Systems toxicology assessment of CHTP1.2 [Lung Data]

2018-04-10 | E-MTAB-6319 | biostudies-arrayexpress

Combined Chronic Toxicity and Carcinogenicity of Aerosol from a Heated Tobacco Product (microRNA data).

Project description:Smoking cessation is the most effective measure for reducing the risk of smoking-related diseases but switching to less harmful products (modified-risk tobacco products) can be an alternative for smokers who would otherwise not quit. In an 18-month chronic carcinogenicity/toxicity study in A/J mice (OECD Test Guideline 453), we assessed the Tobacco Heating System 2.2 (THS 2.2), a candidate modified-risk tobacco product based on the heat-not-burn principle, compared with 3R4F cigarette smoke (CS). To capture toxicity- and disease-relevant mechanisms, we complemented standard toxicology endpoints with in-depth systems toxicology analyses. In this part of our publication series, we report on the integrative assessment of the apical and molecular exposure effects on the respiratory tract (nose, larynx, and lung). Across the respiratory tract, we found differences in the inflammatory response following 3R4F CS exposure (e.g., an antimicrobial peptide response in the nose), and both shared and distinct oxidative and xenobiotic responses. Compared with 3R4F CS, THS 2.2 aerosol exposure exerted far fewer effects on respiratory tract histology, including adaptive tissue changes in nasal and laryngeal epithelium and inflammation and emphysematous changes in the lung. Integrative analysis of the molecular alterations confirmed the substantially lower impact of THS 2.2 aerosol than 3R4F CS on toxicologically and disease-relevant molecular processes such as inflammation, oxidative stress responses, and activation of xenobiotic metabolism. In summary, this work exemplifies how apical and molecular endpoints can be combined effectively for toxicology assessment and further supports reduced respiratory health risks of THS 2.2 aerosol.

2020-08-17 | E-MTAB-8541 | biostudies-arrayexpress

Combined Chronic Toxicity and Carcinogenicity of Aerosol from a Heated Tobacco Product (mRNA data)

2020-08-17 | E-MTAB-8540 | biostudies-arrayexpress

Systems toxicology assessment of CHTP1.2 [Lung Data]

Project description:Modified risk tobacco products (MRTPs) have the potential to reduce smoking-related health risks. The Carbon Heated Tobacco Product 1.2 (CHTP1.2) is a potential MRTP that uses a pressed carbon heat source to generate an aerosol by heating tobacco. This study reports the results from the systems toxicology arm of a 90-day rat inhalation study (OECD test guideline 413) to assess the effects of CHTP1.2 aerosol compared with cigarette smoke (CS). Rats were exposed to filtered air (sham), to CHTP1.2 aerosol (at 15, 23 and 50 Âµg nicotine / L), or to the 3R4F reference cigarette smoke (at 23 Âµg nicotine / L).

2018-03-19 | PXD008422 | Pride

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