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尼古丁促进电子烟蒸气引起的肺部炎症和结构改变
European Respiratory Journal
(
IF
16.6
)
Pub Date : 2023-06-22
, DOI:
10.1183/13993003.00951-2022
Elsa T Roxlau
1,
2
,
Oleg Pak
1,
2
,
Stefan Hadzic
1
,
Claudia F Garcia-Castro
1
,
Marija Gredic
1
,
Cheng-Yu Wu
1
,
Julia Schäffer
1
,
Balachandar Selvakumar
1,
3
,
Alexandra Pichl
1
,
David Spiegelberg
1
,
Janik Deutscher
1
,
Mariola Bednorz
1
,
Katharina Schäfer
1
,
Simone Kraut
1
,
Djuro Kosanovic
1,
4
,
Esraa M Zeidan
1,
5
,
Baktybek Kojonazarov
1,
6
,
Susanne Herold
1
,
Ievgen Strielkov
1
,
Andreas Guenther
1
,
Jochen Wilhelm
1,
6
,
Mohamed M A Khalifa
5
,
Ashraf Taye
7
,
Ralf P Brandes
8
,
Matthias Hecker
1
,
Friedrich Grimminger
1
,
Hossein A Ghofrani
1,
9
,
Ralph T Schermuly
1
,
Werner Seeger
1,
6,
10
,
Natascha Sommer
11
,
Norbert Weissmann
1
Affiliation
- Justus Liebig University, Excellence Cluster Cardio-Pulmonary Institute (CPI), Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Center for Lung Research (DZL), Giessen, Germany.
- Joint first authors.
- Sharjah Institute of Medical Research (SIMR), College of Medicine - University of Sharjah (UoS), Sharjah, United Arab Emirates.
- I.M. Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia.
- Department of Pharmacology and Toxicology, Faculty of Pharmacy, Minia University, El-Minia, Egypt.
- Institute for Lung Health (ILH), Giessen, Germany.
- Department of Pharmacology and Toxicology, Faculty of Pharmacy, South Valley University, Qena, Egypt.
- Institute for Cardiovascular Physiology, Goethe University, Cardio-Pulmonary Institute (CPI), Frankfurt, Germany.
- Department of Medicine, Imperial College London, London, UK.
- Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
- Justus Liebig University, Excellence Cluster Cardio-Pulmonary Institute (CPI), Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Center for Lung Research (DZL), Giessen, Germany
背景
电子烟蒸汽作为吸烟的替代品越来越受欢迎,并且可能引起急性肺损伤。然而,电子烟蒸汽中尼古丁的具体作用及其对气道、肺实质和脉管系统的长期影响仍不清楚。
结果
体外暴露于含尼古丁的电子烟蒸气提取物(ECVE)或不含尼古丁的电子烟蒸气提取物(NF ECVE)会诱导上皮细胞和肺动脉平滑肌细胞(PASMC)的基因表达发生变化,但ECVE特别是引起功能改变(例如人和小鼠PASMC增殖分别减少29.3±5.3%和44.3±8.4%)。此外,急性吸入含尼古丁的电子烟蒸气(ECV)而非不含尼古丁的电子烟蒸气(NF ECV)会增加离体肺部的肺内皮通透性。小鼠长期体内暴露于ECV 8个月,与对照组和NF ECV相比,支气管肺泡液(BALF)中炎症细胞,特别是淋巴细胞的数量显着增加(ECV:853.4±150.8个细胞·mL –1 ;对照:37.0±21.1 个细胞·mL –1 ;NF ECV:198.6±94.9 个细胞·mL –1 )和肺组织(ECV:25.7±3.3 个细胞·mm –3 ;对照:4.8±1.1 个细胞·mm –3 ; NF ECV:14.1±2.2 cells·mm –3 )。 ECV 主要增加 BALF 细胞因子。此外,ECV 引起肺结构和功能的显着变化(例如,与对照相比,空气空间增加 17.5±1.4%),类似于轻度烟草烟雾引起的改变,这也可以在 NF ECV 组中检测到,尽管程度较小程度。相反,肺血管系统并未受到ECV或NF ECV的显着影响。
结论
NF ECV 成分会诱导细胞类型特异性效应和轻微的肺部改变,而尼古丁的包含会诱导显着的内皮损伤、炎症和实质改变。
"点击查看英文标题和摘要"
Nicotine promotes e-cigarette vapour-induced lung inflammation and structural alterations
Background
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.
Results
In vitro exposure to nicotine-containing e-cigarette vapour extract (ECVE) or to nicotine-free e-cigarette vapour extract (NF ECVE) induced changes in gene expression of epithelial cells and pulmonary arterial smooth muscle cells (PASMCs), but ECVE in particular caused functional alterations (e.g. a decrease in human and mouse PASMC proliferation by 29.3±5.3% and 44.3±8.4%, respectively). Additionally, acute inhalation of nicotine-containing e-cigarette vapour (ECV) but not nicotine-free e-cigarette vapour (NF ECV) increased pulmonary endothelial permeability in isolated lungs. Long-term in vivo exposure 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 fluid (BALF) (ECV: 853.4±150.8 cells·mL–1; control: 37.0±21.1 cells·mL–1; NF ECV: 198.6±94.9 cells·mL–1) and in lung tissue (ECV: 25.7±3.3 cells·mm–3; control: 4.8±1.1 cells·mm–3; NF ECV: 14.1±2.2 cells·mm–3). BALF 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.
Conclusions
NF ECV components induce cell type-specific effects and mild pulmonary alterations, while inclusion of nicotine induces significant endothelial damage, inflammation and parenchymal alterations.
更新日期:2023-06-22