Cigarette smoke alters lung vascular permeability and endothelial barrier function (2017 Grover Conference Series)

Rounds, Sharon; Lü, Qing

doi:10.1177/2045894018794000

Cited by 13 publications

(8 citation statements)

References 41 publications

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“…Nicotine could directly alter the function of vascular endothelial cells, PASMC, airway epithelial cells, and immune cells expressing nicotinic acetylcholine receptors [37], thus promoting increased capillary permeability. Although using oil-formulated tetrahydrocannabinol or cannabidiol in ECV was suggested to be associated with vaping-induced ARDS, our data indicate that nicotine in e-cigarettes may contribute to ARDS development [6,7,[36][37][38][39].…”

Section: Due To the Lack Of General Standardisation Of E-cigarette Va...mentioning

confidence: 99%

“…Similarly, cigarette smoke increases the risk of ARDS due to alterations in pulmonary vascular permeability and endothelial barrier function [38]. In addition to endothelial permeability, pulmonary vasoreactivity, in response to acute hypoxia, was affected by e-cigarette vapour, independently from the presence of nicotine.…”

Section: Due To the Lack Of General Standardisation Of E-cigarette Va...mentioning

confidence: 99%

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Nicotine promotes e-cigarette vapour-induced lung inflammation and structural alterations

et al. 2023

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Electronic cigarette (e-cigarette) vapour is gaining popularity as an alternative to tobacco smoking and can induce acute lung injury. However, the specific role of nicotine in e-cigarette vapour and its long-term effects on the airways, lung parenchyma and vasculature remain unclear. We found thatin vitroexposure to nicotine-containing e-cigarette vapour extract (ECVE) or nicotine-free extract (NF ECVE) induced changes in gene expression of epithelial cells and pulmonary arterial smooth muscle cells (PASMC), but preferentially ECVE caused functional alterations (e.g.decrease of human or mouse PASMC proliferation by 29.3±5.3% or 44.3±8.4%, respectively). Additionally, acute inhalation of nicotine-containing e-cigarette vapour (ECV) but not nicotine-free vapour (NF ECV) increased pulmonary endothelial permeability in isolated lungs. Long-term,in vivoexposure of mice to ECV for 8 months significantly increased the number of inflammatory cells, in particular lymphocytes compared to control and NF ECV in the bronchoalveolar lavage (BAL, ECV: 853.4±150.8, control: 37.0±21.1, NF ECV: 198.6±94.9 cells·mL−1) and in lung tissue (ECV: 25.7±3.3, control: 4.8±1.1, NF ECV: 14.1±2.2 cells·mm−3). BAL-cytokines were predominantly increased by ECV. Moreover, ECV caused significant changes in lung structure and function (e.g.increase in airspace by 17.5±1.4% compared to control), similar to mild tobacco smoke-induced alterations, which also could be detected in the NF ECV group, albeit to a lesser degree. In contrast, the pulmonary vasculature was not significantly affected by ECV or NF ECV. In conclusion, NF ECV components induce cell-type specific effects and mild pulmonary alterations, while inclusion of nicotine induces significant endothelial damage, inflammation and parenchymal alterations.

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Section: Due To the Lack Of General Standardisation Of E-cigarette Va...mentioning

confidence: 99%

Section: Due To the Lack Of General Standardisation Of E-cigarette Va...mentioning

confidence: 99%

Nicotine promotes e-cigarette vapour-induced lung inflammation and structural alterations

et al. 2023

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“…Tobacco smoke exposure has also been associated with alterations of vascular permeability and endothelial barrier dysfunction [ 25 ]. Higher cumulative tobacco exposure has been reported in PVOD compared to idiopathic PAH [ 11 ].…”

Section: Risk Factors and Conditions Associated With Pvodmentioning

confidence: 99%

Pulmonary veno-occlusive disease: illustrative cases and literature review

Lechartier,

Boucly,

Solinas

et al. 2024

Eur Respir Rev

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Pulmonary veno-occlusive disease (PVOD), also known as “pulmonary arterial hypertension (PAH) with overt features of venous/capillary involvement”, is a rare cause of PAH characterised by substantial small pulmonary vein and capillary involvement, leading to increased pulmonary vascular resistance and right ventricular failure. Environmental risk factors have been associated with the development of PVOD, such as occupational exposure to organic solvents and chemotherapy, notably mitomycin. PVOD may also be associated with a mutation in theEIF2AK4gene in heritable forms of disease. Distinguishing PVOD from PAH is critical for guiding appropriate management. Chest computed tomography typically displays interlobular septal thickening, ground-glass opacities and mediastinal lymphadenopathy. Life-threatening pulmonary oedema is a complication of pulmonary vasodilator therapy that can occur with any class of PAH drugs in PVOD. Early referral to a lung transplant centre is essential due to the poor response to therapy when compared with other forms of PAH. Histopathological analysis of lung explants reveals microvascular remodelling with typical fibrous veno-occlusive lesions. This review covers the main features distinguishing PVOD from PAH and two clinical cases that illustrate the challenges of PVOD management.

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“…There are over 7000 chemicals in tobacco smoke [7]. Acrolein, one of the cigarette's many carcinogens, has been demonstrated to increase lung vascular permeability by disrupting adherens junctions and actin fibers [8,9]. Other chemicals in cigarette smoke are known to cause cellular insult, which increases the risk of bacterial pneumonia [10,11].…”

Section: Introductionmentioning

confidence: 99%

The effects of smoking on adolescent trauma patients: a propensity-score-matched analysis

et al. 2020

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Purpose Cigarettes have been demonstrated to be toxic to the pulmonary connective tissue by impairing the lung's ability to clear debris, resulting in infection and acute respiratory distress syndrome (ARDS). Approximately 8% of adolescents are smokers. We hypothesized that adolescent trauma patients who smoke have a higher rate of ARDS and pneumonia when compared to non-smokers. Methods The Trauma Quality Improvement Program (2014-2016) was queried for adolescent trauma patients aged 13-17 years. Adolescent smokers were 1:2 propensity-score-matched to non-smokers based on age, comorbidities, and injury type. Data were analyzed using chi square for categorical data and Mann-Whitney U test for continuous data. Results From 32,610 adolescent patients, 997 (3.1%) were smokers. After matching, 459 smokers were compared to 918 non-smokers. There were no differences in matched characteristics. Compared to non-smokers, smokers had an increased rate of pneumonia (3.1% vs. 1.1%, p = 0.01) but not ARDS (0.2% vs. 0%, p = 0.16). Compared to the non-smoking group, the smokers had a longer median total hospital length-of-stay (3 vs. 2 days, p = 0.01) and no difference in overall mortality (1.5% vs. 2.4%, p = 0.29). Conclusion Smoking is associated with an increased rate of pneumonia in adolescent trauma patients. Future research should target smoking cessation and/or interventions to mitigate the deleterious effects of smoking in this population.

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Cigarette smoke alters lung vascular permeability and endothelial barrier function (2017 Grover Conference Series)

Cited by 13 publications

References 41 publications

Nicotine promotes e-cigarette vapour-induced lung inflammation and structural alterations

Nicotine promotes e-cigarette vapour-induced lung inflammation and structural alterations

Pulmonary veno-occlusive disease: illustrative cases and literature review

The effects of smoking on adolescent trauma patients: a propensity-score-matched analysis

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