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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 [Heart iTRAQ data].

ABSTRACT: 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 heart using the iTRAQ® quantification approach.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart

SUBMITTER: Bjoern Titz

LAB HEAD: Julia Hoeng

PROVIDER: PXD010873 | Pride | 2022-02-23

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	20171013_S186500__HEART-B_setM3_1_DR_PS_01.raw	Raw
	20171013_S186500__HEART-B_setM3_1_DR_PS_13.raw	Raw
	20171013_S186500__HEART-B_setM3_3_DR_PS_08.raw	Raw
	20171013_S186500__HEART-B_setM3_3_DR_PS_20.raw	Raw
	20171013_S186500__HEART-B_setM3_5_DR_PS_05.raw	Raw

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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.

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Systems toxicology assessment of CHTP1.2 [Liver Data]

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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).

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2018-03-19 | PXD008424 | Pride

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.

2019-04-18 | E-MTAB-7444 | biostudies-arrayexpress

2019-04-18 | E-MTAB-7892 | biostudies-arrayexpress

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.

2015-11-30 | PXD002530 | Pride

Impact of whole-body versus nose-only exposure systems on systemic, respiratory, and cardiovascular endpoints in a 2-month cigarette smoke exposure study in the ApoE-/- mouse model

Project description:In vivo inhalation toxicity is typically tested in rodents by using either whole-body (WB) or nose-only (NO) exposure systems. To assess if cigarette smoke (CS)-induced disease endpoints would be similar after exposure in either system, we exposed apolipoprotein E-deficient mice to the same target total particulate matter concentration of mainstream smoke from 3R4F reference cigarettes in NO or WB exposure chambers (EC) for 2 months, and as controls to filtered air (Sham). While CS was reproducibly delivered to both exposure systems, we observed higher nicotine and formaldehyde concentrations being delivered to NOECs than to WBECs, but similar concentrations of carbon monoxide, acetaldehyde, and acrolein. CS exposure led to the adaptive changes expected in nasal epithelia, altered lung function, increased lung inflammation, and pronounced changes in the nasal epithelial transcriptome and lung proteome. Exposure in the NOEC caused generally more pronounced or severe respiratory effects and a higher stress response. Body weight, in particular, was much lower in mice exposed in the NOEC. Aortic arch imaging revealed greater plaque area in CS-exposed mice in the WBEC group than in the respective sham group. No difference was found in aortic plaque size between CS-exposed mice in the NOEC and sham groups. As CS is a chemically and temporarily dynamic aerosol, its composition in the breathing zone was not completely comparable between the two exposure systems; however, the main disease endpoints and exposure effects were largely induced in both systems. NO exposure appeared to be more stressful for the mice than WB exposure.

2021-03-16 | E-MTAB-9248 | 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).

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