Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Data from Pregnancy exacerbates neutrophil responses in murine lungs and alters gut microbiota composition after cigarette smoke exposure

ABSTRACT: Air pollution, particularly environmental tobacco smoke, poses significant health risks, especially to pregnant women and their infants. This study explores the difference in response to cigarette smoke (CS) exposure between pregnant and non-pregnant mice by examining lung transcriptomic profiles, neutrophil numbers, key mediators of neutrophil chemotaxis, and gut microbiota composition. Pregnant and non-pregnant mice were exposed to either air or CS. Bronchoalveolar lavage fluid (BALF) was analyzed for inflammatory cells and mediators. RNA sequencing was conducted on lung tissue to identify transcriptomic alterations.

ORGANISM(S): Mus musculus

PROVIDER: GSE302905 | GEO | 2025/07/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Alveolar type II epithelial cell FASN maintains lipid homeostasis in experimental COPD

Project description:Alveolar epithelial type II cells (AEC2) strictly regulate lipid metabolism to maintain surfactant synthesis. A loss in AEC2 cell function and surfactant production are implicated in the pathogenesis of the smoking related lung disease, chronic obstructive pulmonary disease (COPD). It is unclear if smoking alters lipid synthesis in AEC2 cells and if altering lipid metabolism in AEC2 cells contributes to COPD development. In this study, high throughput lipidomic analysis revealed increased lipid biosynthesis in AEC2 cells isolated from mice chronically exposed to cigarette smoke (CS). Mice with a targeted deletion of the de novo lipogenesis enzyme, fatty acid synthase (FASN) in AEC2 cells (FasniAEC2) exposed to CS exhibited higher bronchoalveolar lavage fluid (BALF) neutrophils, higher BALF protein, more severe air-space enlargement and were more susceptible to age-induced emphysema. FasniAEC2 mice exposed to CS had lower levels of key surfactant phospholipids but higher levels of BALF ether phospholipids, sphingomyelins and polyunsaturated fatty acid containing-phospholipids, as well as increased BALF surface tension. FasniAEC2 mice exposed to CS also had higher markers of ferroptosis in the lung. These data suggest that AEC2 cell FASN modulates the response of the lung to smoke by regulating the composition of the surfactant phospholipidome.

2023-08-22 | GSE235644 | GEO

Effect of cessation after initial exposure to cigarette smoke

Project description:Although smoking cessation shows clear cardiovascular risk benefits, lung-related disease risk remains higher in former smokers than in never smokers. To better understand the factors involved in this phenomenon, ApoE-/- mice were exposed to mainstream cigarette smoke (CS) or a smoking cessation-mimicking protocol for up to six months. Analysis of bronchoalveolar lavage fluid (BALF) from CS-exposed ApoE-/- mice revealed the presence of high concentrations of mediators involved in functions ranging from inflammation to cell proliferation and tissue remodeling. Gene expression levels for many analytes found elevated in BALF were also increased in lung tissue, indicating that the inflammatory response was the result of local tissue activation and the contribution of recruited inflammatory cells. Gene set enrichment analysis (GSEA) of expression data from lungs of CS-exposed mice showed activation of pathways involved in cell proliferation and tissue remodeling and a progressive deactivation upon smoke exposure cessation. Distinct activation patterns of inflammation, complement, and xenobiotic metabolism pathways were found in nasal epithelium and lung parenchyma during CS exposure and smoking cessation. Exposure of ApoE-/- mice to CS for up to 6 months induced adaptive and inflammatory responses in the respiratory tract that were partially deactivated upon cessation. We were able to reveal molecular perturbations accompanying these changes during CS exposure and cessation. Differential CS-mediated responses of pulmonary and nasal tissues reflect common mechanisms but also the varying degrees of epithelial functional specialization along the respiratory tract. These findings provide novel clues for the identification of markers of COPD progression.

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

Angiotensin receptor blockade attenuates cigarette smoke-induced lung injury and rescues lung architecture in a murine model

Project description:TGFβ inhibition attenuates chronic cigarette smoke induced lung injury and rescues lung architecture. AKR/J mice were exposed to Cigarette Smoke (CS) for a period of two months. Some animals received a treatment of Losartan (.6gr/L) orally while exposed (CS Los). These two groups are to be compared to animals that remained in Room Air (RA) and Room Air plus Losartan(0.6g/L) (RA Los) for any changes.

2011-12-30 | E-GEOD-33561 | biostudies-arrayexpress

Label free DIA proteomic analysis of thoracic lymph from cigarette smoke (CS)-exposed mice

Project description:The lymphatic vasculature is critical for lung function, but defects in lymphatic functionin the pathogenesis of lung disease is understudied. To further assess the contribution of lymphatics to the pathogenesis of lung emphysema we used a mouse model of cigarette smoke (CS)-induced emphysema, and analyzed lung lymphatics using immunohistochemistry, functional assays, and confocal microscopy. Additionally, we further harvested thoracic lymph from CS-exposed mice for proteomic analysis. In this presented section of our research, we highlight the label free quantitative DIA proteomics approaches used to profile the proteomic and peptidomics changes in the lymph from cigarette smoke (CS)-mice as compared with the lymph proteome from mice exposed to room air. Label free quantitative DIA proteomics analysis of lymph confirmed upregulation of coagulation and inflammatory pathways in the lymphatics of CS-exposed mice compared to control mice.

2022-05-10 | PXD031413 | Pride

An In Vitro Versus In Vivo Toxicogenomics Investigation of Pre-natal Exposures to Tobacco Smoke [Dams, Prenatal offspring]

Project description:Pregnant mice (Dams) were exposed to cigarette smoke or filtered air. Lung tissue and RNA were harvested from the lungs of the Dams and their offspring and underwent transcriptomic analysis.

2017-04-03 | GSE96977 | GEO

Effects of mitochondria-targeted antioxidant SS-31 on cigarette smoke-induced airway inflammation and oxidative stress in a mouse model

Project description:This study investigated whether mitochondria-targeted peptide SS-31 played a protective role in cigarette smoke (CS)-induced airway inflammation and oxidative stress in mice. Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, then treated with SS-31. Pathological changes and oxidative stress in lung tissue, inflammatory cell counts and pro-inflammatory cytokines in bronchoalveolar lavage fluid (BALF) were examined. RNA sequencing from lung tissue and western blotting were conducted to investigate mechanisms. SS-31 attenuated CS-induced inflammatory injury of the airway. Numbers of total cells, neutrophils, and macrophages and levels of tumor necrosis factor α, interleukin 6, and matrix metallopeptidase 9 in BALF were markedly reduced by SS-31. SS-31 attenuated CS-induced oxidative stress by decresing malondialdehyde and myeloperoxidase levels, and increasing superoxide dismutase activity. It also reversed the expression of mitochondrial fission protein and optic atrophy 1 protein, and reduced cytochrome c release into the cytosol. RNA sequencing revealed that SS-31 changed CS-induced expression profiles and enriched MAPK pathway, western blotting confirmed that SS-31 inhibited the CS-activated MAPK pathway. SS-31 alleviates CS-induced airway inflammation and oxidative stress, possibly via the regulation of mitochondrial function and MAKP pathway, SS-31 may be a novel drug for CS-induced airway disorders.

2020-12-25 | GSE163835 | GEO

Organotypic human bronchial epithelial cultures (MucilAir) exposed to mainstream aerosols from the 3R4F cigarette and a novel tobacco vapor product

Project description:Cigarette smoke (CS) is an aerosol containing more than 6,000 chemicals and one of the risk factor in the development of chronic inflammatory lung disease. To evaluate biological effect of CS on human respiratory tract, organotypic bronchial epithelial cultures can be used to replicate in vivo tissue conditions. The MucilAir organotypic bronchial epithelial cultures were exposed to mainstream aerosols from the 3R4F cigarette and a novel tobacco vapor product (NTV), which we recently developed, using a Vitrocell exposure system. This system consists of three steps: the generation of CS, dilution, and exposure to an air-liquid interface cultured cells in a specially designed module. This exposure scenario mimics CS exposure in the human airway (i.e. direct aerosol exposure to the apical surface of air-liquid interface-cultured cells), We found a dose-dependent increase in the number of differentially expressed genes following 3R4F cigarette smoke exposure, compared with expression in air-exposed controls. In contrast, no changes were detected following exposure to NTV vapor.

2018-02-09 | E-MTAB-6471 | biostudies-arrayexpress

NHBE exposed to cigarette smoke

Project description:normal human bronchial epithelial cultures from two cultures in parallel exposed to cigarette smoke (CS) or air (mock) at timepoints 4 hours and 24 hours. Keywords = cigarette smoke Keywords = microarray Keywords = bronchial cell Keywords = tobacco Keywords: time-course

2005-02-23 | GSE2302 | GEO

In Utero Cigarette Smoke Affects Allergic Airway Disease But Does Not Alter the Lung Methylome

Project description:Introduction: Prenatal and postnatal cigarette smoke exposure enhances the risk of developing asthma. Despite this as well as other smoking related risks, 11% of women still smoke during pregnancy. We hypothesized that cigarette smoke exposure during prenatal development generates long lasting differential methylation altering transcriptional activity that correlates with disease. Methods: In a house dust mite (HDM) model of allergic airway disease, we measured airway hyperresponsiveness (AHR) and airway inflammation between mice exposed prenatally to cigarette smoke (CS) or filtered air (FA). DNA methylation and gene expression were then measured in lung tissue. Results: We demonstrate that HDM-treated CS mice develop a more severe allergic airway disease compared to HDM-treated FA mice including increased AHR and airway inflammation. While DNA methylation changes between the two HDM-treated groups failed to reach genome-wide significance, 99 DMRs had an uncorrected p-value < 0.001. 6 of these 99 DMRs were selected for validation, based on the immune function of adjacent genes, and only 2 of the 6 DMRs confirmed the bisulfite sequencing data. Additionally, genes near these 6 DMRs (Lif, Il27ra, Tle4, Ptk7, Nfatc2, and Runx3) are differentially expressed between HDM-treated CS mice and HDM-treated FA mice. Conclusions: Our findings confirm that prenatal exposure to cigarette smoke is sufficient to modify allergic airway disease, however, it is unlikely that specific methylation changes account for the exposure-response relationship. These findings highlight the important role in utero cigarette smoke exposure plays in the development of allergic airway disease. Lung DNA methylation profiles of mice exposed in utero to cigarette smoke (CS) then treated with house dust mite (HDM, n = 8) or saline (n = 6), or exposed in utero to filtered air (FA) then treated with HDM (n = 9) or saline (n = 6)

2015-11-19 | E-GEOD-71718 | biostudies-arrayexpress

Tobacco smoke exposure exacerbates silica-induced pulmonary toxicity in rats

Project description:Previous studies have shown that smoking induces oxidative stress and inflammation, known factors that coincide with the development and progression of silicosis. Nevertheless, the precise role of cigarette smoke exposure in silicosis and the underlying mechanisms are not clearly understood. Therefore, the objective of the present study was to determine the effect of smoking, if any, on silica-induced pulmonary response and the underlying mechanisms. Pulmonary toxicity and lung gene expression profiles were determined in male Fischer 344 rats exposed to air, crystalline silica, cigarette smoke or cigarette smoke plus crystalline silica. Silica exposure resulted in significant pulmonary toxicity which was further exacerbated by cigarette smoke exposure in the rats. Significant differences in the gene expression profiles were detected in the lungs of the rats exposed to cigarette smoke, silica or a combination of both compared with the control rats.

2020-11-01 | GSE136945 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data