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Apoe-/- mouse gut microbiome

ABSTRACT: Impact of 6-Month Exposure to Aerosols from Potential Modified Risk Tobacco Products Relative to Cigarette Smoke on the Rodent Gastrointestinal Tract

PROVIDER: PRJEB39465 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4364500_1.fastq.gz	Fastqsanger.gz
	ERR4364500_2.fastq.gz	Fastqsanger.gz
	ERR4366970_1.fastq.gz	Fastqsanger.gz
	ERR4366970_2.fastq.gz	Fastqsanger.gz
	ERR4366980_1.fastq.gz	Fastqsanger.gz

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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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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.

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A 7-month inhalation toxicology study in C57BL/6 mice demonstrates reduced pulmonary inflammation and emphysema following smoking cessation or switching to e-vapor products.

Project description:Cigarette smoking causes serious diseases, including lung cancer, heart disease, and emphysema. While cessation remains the most effective approach to minimize smoking-related disease, alternative non-combustible tobacco-derived nicotine containing products may reduce disease risks among those unable or unwilling to quit. E-vapor aerosols typically contain significantly lower levels of smoke-related harmful and potentially harmful constituents; however, health risks of long-term inhalation exposures are unknown. We designed a 7-month inhalation study in C57BL/6 mice to evaluate long-term respiratory toxicity of e-vapor aerosols compared to cigarette smoke and to assess the impact of smoking cessation or switching to an e-vapor product after 3 months of exposure to 3R4F cigarette smoke (CS). There were no significant changes in in-life observations (body weights, clinical signs) in e-vapor groups compared to the Sham Control. The 3R4F CS group showed reduced respiratory function during exposure and had lower body weight and showed transient signs of distress post-exposure. Following 7 months of exposure, e-vapor aerosols resulted in no or minimal increase in pulmonary inflammation, while exposure to 3R4F CS led to impairment of lung function and caused marked lung inflammation and emphysematous changes. Biological changes observed in the Switching group were similar to the Cessation group. 3R4F CS exposure dysregulated lung and nasal tissue transcriptome, while these molecular effects were substantially lower in the e-vapor group. Results from this study demonstrate that in comparison with 3R4F CS, e-vapor aerosols induce substantially lower biological responses including pulmonary inflammation and emphysema, and that complete switching from CS to e-vapor products significantly reduces biological changes associated with cigarette smoke in C57BL/6 mice.

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Project description: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.

2020-04-25 | MTBLS158 | MetaboLights

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 [Liver 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 liver using the iTRAQ® quantification approach.

2022-02-23 | PXD010874 | Pride

2019-06-18 | PXD010875 | Pride

2022-02-23 | PXD010873 | Pride

Systems toxicology assessment of CHTP1.2 [Liver 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).

2018-03-19 | PXD008423 | Pride

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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