Nicotinic receptors atlas in the adult human lung

Diabasana, Zania; Perotin-Collard, Jeanne-Marie; Belgacemi, Randa; Ancel, Julien; Mulette, Pauline; Delépine, G.; Gosset, Philippe; Maskos, Uwe; Polette, Myriam; Deslée, G.; Dormoy, Valérian

doi:10.1101/2020.06.29.176750

Cited by 6 publications

(1 citation statement)

References 51 publications

(58 reference statements)

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“…Interestingly, only ECV but not NF ECV increased capillary permeability, indicating the effect of nicotine. 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%

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%

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

et al. 2023

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Lower Gene Expression of Angiotensin Converting Enzyme 2 Receptor in Lung Tissues of Smokers with COVID-19 Pneumonia

et al. 2021

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Angiotensin-converting enzyme 2 (ACE-2) is the main cell entry receptor for severe acute respiratory syndrome-Coronavirus-2 (SARS-CoV-2), thus playing a critical role in causing Coronavirus disease 2019 (COVID-19). The role of smoking habit in the susceptibility to infection is still controversial. In this study we correlated lung ACE-2 gene expression with several clinical/pathological data to explore susceptibility to infection. This is a retrospective observational study on 29 consecutive COVID-19 autopsies. SARS-CoV-2 genome and ACE-2 mRNA expression were evaluated by real-time polymerase chain reaction in lung tissue samples and correlated with several data with focus on smoking habit. Smoking was less frequent in high than low ACE-2 expressors (p = 0.014). A Bayesian regression also including age, gender, hypertension, and virus quantity confirmed that smoking was the most probable risk factor associated with low ACE-2 expression in the model. A direct relation was found between viral quantity and ACE-2 expression (p = 0.028). Finally, high ACE-2 expressors more frequently showed a prevalent pattern of vascular injury than low expressors (p = 0.049). In conclusion, ACE-2 levels were decreased in the lung tissue of smokers with severe COVID-19 pneumonia. These results point out complex biological interactions between SARS-CoV-2 and ACE-2 particularly concerning the aspect of smoking habit and need larger prospective case series and translational studies.

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Pathophysiology, Therapeutic Targets, and Future Therapeutic Alternatives in COPD: Focus on the Importance of the Cholinergic System

Gomes

Cheng

2023

Biomolecules

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Chronic obstructive pulmonary disease (COPD) is a progressive disease characterized by airway limitation and changes in airway structure. It has a high global burden of mortality and morbidity. The etiology of COPD is complex, but exposure to tobacco smoke and other inhaled lung oxidants are major risk factors. Both pharmacological and non-pharmacological approaches are used to manage COPD, but there remains an urgent unmet need for drugs that can modify the course of the disease. This review focuses on the role of acetylcholine and other components of the pulmonary cholinergic system in the pathogenesis of COPD, and the inhaled pharmacological agents that target it. In addition to its role as a neurotransmitter, acetylcholine regulates diverse aspects of COPD pathogenesis including bronchoconstriction, airway remodeling, mucus secretion and inflammation. Inhaled antimuscarinic drugs are a key component of therapy for COPD, as monotherapy or in combination with inhaled β2 agonists or corticosteroids. We review the evidence supporting the use of current anticholinergic agents in COPD and preview novel drugs targeting the cholinergic system and agents from other classes in clinical development, such as phosphodiesterase-4 inhibitors and monoclonal antibodies targeting inflammatory mediators.

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Nicotinic receptors atlas in the adult human lung

Cited by 6 publications

References 51 publications

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

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

Lower Gene Expression of Angiotensin Converting Enzyme 2 Receptor in Lung Tissues of Smokers with COVID-19 Pneumonia

Pathophysiology, Therapeutic Targets, and Future Therapeutic Alternatives in COPD: Focus on the Importance of the Cholinergic System

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