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Multi-omics systems toxicology study of mouse lung assessing the effects of aerosols from two heat-not-burn tobacco products and cigarette smoke

ABSTRACT: Cigarette smoke (CS) causes adverse health effects and leads to the development of respiratory disease (chronic obstructive pulmonary disease), cardiovascular disease, and cancer. To reduce the risk of smokers developing smoking-related diseases, Philip Morris International is developing modified risk tobacco products (MRTP). Within a systems toxicology study, we conducted an integrative multi-omics analysis to assess the effects of aerosols from two potential MRTPs - the Carbon Heated Tobacco Product (CHTP) 1.2 and the Tobacco Heating System (THS) 1.2 -, compared with cigarette smoke (CS) at matched nicotine concentrations, on the lung of ApoE-/- mice. Mice were exposed for up to six months and molecular exposure effects were measured by mRNA/miRNA transcriptomics, proteomics, metabolomics, and lipidomics. In addition, the impact of cessation (CESS) or switching to CHTP 1.2 (SWITCH) after three months of CS exposure was evaluated. This data set represents the lung metabolomics data obtained after 3 and 6 months of exposure. The 'Animal ID' or 'CAN' represents the unique animal identifier and allows matching of samples across the different data modalities.

OTHER RELATED OMICS DATASETS IN: PXD010875

INSTRUMENT(S): Q Exactive

SUBMITTER: Bjoern Titz

PROVIDER: MTBLS158 | MetaboLights | 2020-04-25

REPOSITORIES: MetaboLights

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A 6-Month Systems Toxicology Inhalation/Cessation Study in ApoE-/- Mice to Investigate Cardiovascular and Respiratory Exposure Effects of the Modified-Risk Tobacco Products CHTP1.2 and THS2.2 Compared with the Effects of Conventional Cigarettes [Lung iTRAQ data].

Project description:Cigarette smoke (CS) causes adverse health effects that may occur shortly after smoking initiation and lead to the development of respiratory disease (chronic obstructive pulmonary disease), cardiovascular disease, and cancer. To reduce the risk of smokers developing smoking-related diseases, Philip Morris International is developing modified risk tobacco products (MRTP). Within a systems toxicology study, we integrated multi-omics measurements with classical endpoints to assess the effects in female ApoE-/- mice of six months of exposure to CS (at 29.9 µg nicotine/L) or to aerosols from one potential and one candidate MRTP (CHTP 1.2 and THS 2.2, respectively) at matched nicotine concentrations. The impact of cessation or switching to CHTP 1.2 after three months of CS exposure was also evaluated. This data set contains the results from the analysis of proteome changes in the lung using the iTRAQ® quantification approach.

2019-06-18 | PXD010875 | Pride

2022-02-23 | PXD010873 | Pride

2022-02-23 | PXD010874 | Pride

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).

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A Six-Month Systems Toxicology Inhalation/Cessation Study in ApoE-/- Mice to Investigate Cardiovascular and Respiratory Exposure Effects of Modified Risk Tobacco Products, CHTP 1.2 and THS 2.2, Compared with Conventional Cigarettes

Project description:Smoking is one of the major modifiable risk factors in the development and progression of chronic obstructive pulmonary disease (COPD) and cardiovascular disease (CVD). Modified-risk tobacco products (MRTP) are being developed to provide substitute products for smokers who are unable or unwilling to quit, to lessen the smoking-related health risks. In this study, the ApoE-/- mouse model was used to investigate the impact of cigarette smoke (CS) from the reference cigarette 3R4F, or aerosol from two potential MRTPs based on the heat-not-burn principle, carbon-heated tobacco product 1.2 (CHTP 1.2) and tobacco heating system 2.2 (THS 2.2), on the cardiovascular and respiratory system over a 6-month period. In addition to chronic exposure, cessation or switching to CHTP1.2 after 3 months of CS exposure was assessed. A systems toxicology approach combining physiology, histology and molecular measurements (transcriptomics and proteomics) was used to evaluate the impact of MRTP aerosols in comparison to CS. The current data represent the lung transcriptomics analysis. Note that the animal identifier (CAN) can be used for sample matching across different sample types and data modalities.

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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

COPD progression in c57bl/6 mice

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.

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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.

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Use of Apoe−/− Mice in an 8-Month Systems Toxicology Inhalation/Cessation Study to Investigate Cardiovascular and Respiratory Exposure Effects of 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 cardiovascular disease (CVD) and chronic obstructive pulmonary disease (COPD), so modified risk tobacco products (MRTPs) are being developed to reduce smoking-related health risks. The present study investigated the hallmarks of COPD and CVD over an 8-month period in apolipoprotein E-deficient 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 was investigated. In a systems toxicology approach, exposure effects were investigated using physiology and histology combined with transcriptomics, lipidomics, and proteomics. CS induced nasal epithelial hyperplasia and metaplasia, lung inflammation, and emphysematous changes (impaired pulmonary function and alveolar damage). Atherogenic effects of CS exposure included altered lipid profiles and increased aortic plaque formation. Exposure to THS2.2 aerosol (nicotine concentration matched to CS: 29.9 mg/m3) did not induce lung inflammation or emphysema, nor did it consistently change the lipid profile or enhance the plaque area. Cessation and switching reversed the inflammatory responses and led to no further progression of initial emphysematous changes or the aortic plaque area. Biological processes, including senescence, inflammation, and proliferation, were significantly impacted in CS, but not THS2.2-exposed tissues. Cessation or switching reduced these perturbations to become nearly indistinguishable from sham exposure. In conclusion, this mouse model indicated that cessation or switching to THS2.2 retarded the progression of atherosclerotic and emphysematous changes, while THS2.2 alone had no adverse effects.

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