The impact of tobacco smoke exposure and environmental exposures on the pulmonary microbiome of critically ill children
Ontology highlight
ABSTRACT:
ORGANISM(S): Human Homo Sapiens
TISSUE(S): Urine
SUBMITTER: 
Karan Uppal
PROVIDER: ST001262 | MetabolomicsWorkbench | Tue Jun 25 00:00:00 BST 2019
REPOSITORIES: MetabolomicsWorkbench
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Project description:Background: Healthy individuals exposed to low levels of cigarette smoke have a decrement in lung function and higher risk for lung disease compared to unexposed individuals. We hypothesized that healthy individuals exposed to low levels of tobacco smoke must have biologic changes in the small airway epithelium compared to healthy unexposed individuals. Methods: Small airway epithelium was obtained by bronchoscopy from 121 individuals; microarrays assessed genome wide gene expression, and urine nicotine and cotinine were used to categorized subjects as “nonsmokers,” “active smokers,” and “low exposure.” The gene expression data was used to determine the threshold and ID50 of urine nicotine and cotinine at which the small airway epithelium showed abnormal responses. Results: There was no threshold of urine nicotine without an abnormal small airway epithelial response, and only a slightly above detectable threshold abnormal response for cotinine. The nicotine ID50 for nicotine was 25 ng/ml and cotinine 104 ng/ml. Conclusions: The small airway epithelium detects and responds to low levels of tobacco smoke with transcriptome modifications. This provides biologic correlates of epidemiologic studies linking low level tobacco smoke exposure to lung health risk, health, identifies genes in the lung cells most sensitive to tobacco smoke and defines thresholds at the lung epithelium responds to inhaled tobacco smoke.
2011-02-02 | GSE19667 | GEO
Project description:Background: Healthy individuals exposed to low levels of cigarette smoke have a decrement in lung function and higher risk for lung disease compared to unexposed individuals. We hypothesized that healthy individuals exposed to low levels of tobacco smoke must have biologic changes in the small airway epithelium compared to healthy unexposed individuals. Methods: Small airway epithelium was obtained by bronchoscopy from 121 individuals; microarrays assessed genome wide gene expression, and urine nicotine and cotinine were used to categorized subjects as “nonsmokers,” “active smokers,” and “low exposure.” The gene expression data was used to determine the threshold and ID50 of urine nicotine and cotinine at which the small airway epithelium showed abnormal responses. Results: There was no threshold of urine nicotine without an abnormal small airway epithelial response, and only a slightly above detectable threshold abnormal response for cotinine. The nicotine ID50 for nicotine was 25 ng/ml and cotinine 104 ng/ml. Conclusions: The small airway epithelium detects and responds to low levels of tobacco smoke with transcriptome modifications. This provides biologic correlates of epidemiologic studies linking low level tobacco smoke exposure to lung health risk, health, identifies genes in the lung cells most sensitive to tobacco smoke and defines thresholds at the lung epithelium responds to inhaled tobacco smoke. Affymetrix arrays were used to assess the gene expression data of smoking-responsive genes in the in small airway epithelium obtained by fiberoptic bronchoscopy of 48 healthy non-smokers (non-smoker or Nsaets), 65 healthy smokers (smoker), 7 symptomatic smokers (SYMs) and a healthy occasional smoker (OcSs). YSB and LO contributed equally to the study.
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Project description:Background: In utero smoke exposure is a recognized risk factor for impaired lung function development and a significant risk factor for airway disease. Despite intensive anti-tobacco campaigns the prevalence of smoking pregnant women has remained high requiring additional strategies to protect the offspring’s lung. To achieve this goal, it is critical to understand the mechanisms how disease risks are established in early life. Objective: To develop an animal model that recapitulates clinical findings in prenatally exposed children to allow the investigation of early molecular changes in the lung. Methods: Pregnant mice were exposed to active smoking from gestational day (GD) 2.5 until caesarean section or spontaneous delivery. After careful maternal characterization, we monitored weight development, lung function, and airway remodeling in offspring. mRNA/miRNA arrays were performed in fetal lungs (GD18.5), followed by network analyses, qPCR and histone analyses.
2019-09-25 | GSE67886 | GEO
Project description:Background: In utero smoke exposure is a recognized risk factor for impaired lung function development and a significant risk factor for airway disease. Despite intensive anti-tobacco campaigns the prevalence of smoking pregnant women has remained high requiring additional strategies to protect the offspring’s lung. To achieve this goal, it is critical to understand the mechanisms how disease risks are established in early life. Objective: To develop an animal model that recapitulates clinical findings in prenatally exposed children to allow the investigation of early molecular changes in the lung. Methods: Pregnant mice were exposed to active smoking from gestational day (GD) 2.5 until caesarean section or spontaneous delivery. After careful maternal characterization, we monitored weight development, lung function, and airway remodeling in offspring. mRNA/miRNA arrays were performed in fetal lungs (GD18.5), followed by network analyses, qPCR and histone analyses.
2019-09-25 | GSE67883 | GEO
Project description:Purpose: Globally, many jurisdictions are legalizing or decriminalizing cannabis, creating a potential public health issue that would benefit from experimental evidence to inform policy, government regulations, and user practices. Tobacco smoke exposure science has created a body of knowledge that demonstrates the conclusive negative impacts on respiratory health; similar knowledge remains to be established for cannabis. To address this unmet need, we performed in vitro functional and transcriptomic experiments with a human airway epithelial cell line (Calu-3) exposed to cannabis smoke, with tobacco smoke as a positive control. Results: We demonstrate that cannabis smoke induced functional and transcriptional responses that overlapped with tobacco smoke. Ontology and pathway analysis revealed that cannabis smoke induced DNA replication and oxidative stress responses. Functionally, cannabis smoke impaired epithelial cell barrier function, antiviral responses, and increased inflammatory mediator production. Our study reveals striking similarities between cannabis and tobacco smoke exposure on impairing barrier function, suppressing antiviral pathways, potentiating of pro-inflammatory mediators, and inducing oncogenic and oxidative stress gene expression signatures. LABA/GC intervention in airway epithelial cells exposed to cannabis smoke reduces levels of pro-inflammatory (CXCL8) and antiviral (CXCL10) mediators, while transcriptomic signatures of neutrophil mediated immunity and oxidative stress remain elevated. Conclusions: Collectively our data suggest that cannabis smoke exposure is not innocuous and may possess many of the deleterious properties of tobacco smoke, warranting additional studies to support public policy, government regulations, and user practices.
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Project description:Previous reports showed that cigarette smoke exposed normal-appearing airways in phenotypically lung cancer-free smokers carry alterations that are characteristic of tumors – suggestive of an airway field of injury. Very little is known of the effects of the chronic consumption of other forms of tobacco, such as waterpipe smoke (WPS), on lung pathobiology. Here we studied normal-appearing airway brushings from waterpipe smokers and those who were not exposed to WPS. We find that WPS elicits a molecular field of injury with gene programs that are pertinent to lung carcinogenesis.
2022-07-13 | GSE197653 | GEO
Project description:Exposure to secondhand tobacco smoke during early childhood has been linked with an increased risk for behavioral disorders, yet little is known regarding how brain development is impacted. Using an environmental tobacco smoke (ETS) passive inhalation model, this study assesses the neurodevelopmental impact of juvenile exposure during a critical period of frontal cortex development, specifically that of the rat orbital neocortex between postnatal days 8 and 22. Agnostic shotgun proteomics was employed to discern the biomolecular shift within this rapidly developing brain region that is responsible for higher-order behavioral control. The orbital cortex neuroproteome was assessed between ETS-exposed and room-air control animals employing a label-free shotgun approach with data-independent acquisition. Following protein roll-up, a total of X protein were found statistically altered in quantity out of Y total proteins identified. These results implicate a prominent shift within metabolic processes and synaptic organization related to excitatory and inhibitory neurotransmission. Findings derived from this dataset may further our understanding of how secondhand smoke exposure can perturb the orbital frontal cortex and result in developmental behavioral disorders.
2018-12-17 | PXD011744 | Pride
Project description:Exposure to secondhand tobacco smoke during early childhood has been linked with an increased risk for behavioral disorders, yet little is known regarding how brain development is impacted. Using an environmental tobacco smoke (ETS) passive inhalation model, this study assesses the neurodevelopmental impact of juvenile exposure during a critical period of frontal cortex development, specifically that of the rat orbital neocortex between postnatal days 8 and 22. Agnostic shotgun proteomics was employed to discern the biomolecular shift within this rapidly developing brain region that is responsible for higher-order behavioral control. The orbital cortex neuroproteome was assessed between ETS-exposed and room-air control animals employing a label-free shotgun approach with data-independent acquisition. Following protein roll-up, a total of X protein were found statistically altered in quantity out of Y total proteins identified. These results implicate a prominent shift within metabolic processes and synaptic organization related to excitatory and inhibitory neurotransmission. Findings derived from this dataset may further our understanding of how secondhand smoke exposure can perturb the orbital frontal cortex and result in developmental behavioral disorders.
2020-05-26 | PXD007690 | Pride
Project description:40 current smokers and 40 age- and gender- matched never smokers underwent buccal biopsies.The study had four objectives: (a) to define the effects of smoking on the transcriptome of oral epithelial cells; (b) to determine if any of the effects of tobacco smoke on the transcriptome are gender-dependent; (c) to compare the effects of tobacco smoke exposure on the transcriptome in oral v. bronchial epithelium and (d) to identify agents with the potential to suppress the effects of tobacco smoke on the transcriptome. We used microarrays to provide new insights into the carcinogenic effects of tobacco smoke and offer insights that may prove useful in developing preventive strategies.
2010-02-15 | GSE17913 | GEO
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