Alveolar Epithelial Cell Dysfunction Induced By Flavored E-Cigarette Aerosols

加味电子烟气雾剂引起的肺泡上皮细胞功能障碍

基本信息

批准号：
10770080
负责人：
Beata Kosmider
金额：
$ 15.85万
依托单位：
TEMPLE UNIV OF THE COMMONWEALTH
依托单位国家：
美国
项目类别：
财政年份：
2023
资助国家：
美国
起止时间：
2023-09-01 至 2025-08-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10770080
关键词：
Administrative Supplement Aerosols Alveolar Cell Death Cell Death Induction Cell Separation Centers for Disease Control and Prevention (U.S.)Cessation of life Cinnamon - dietary Computer Models DNA Damage Data Devices Distal Electronic cigarette Epithelial Cells Epithelium Exposure to Family Female Flavoring Food Fruit Functional disorder Gases Gender Goals Grant Histones Hot Spot Human Incidence Ingestion Inhalation Knowledge Location Lung Mitochondria Mitochondrial DNA National Institute of Environmental Health Sciences Nicotine Nuclear Outcome Parents Particulate Persons Phase Predisposition Production Proliferating Propylene Glycols Publishing Pulmonary Surfactants Reporting Research Respiration Respiratory Disease Risk Sample Size Sex Differences Structure Surface Tension Time Toxic effect Woman alveolar epithelium alveolar type II cell cell injury e-cigarette aerosols electronic cigarette use electronic liquid epithelial repair inflammatory lung disease injured airway lung health lung injury lung regeneration male men mitochondrial dysfunction mitochondrial metabolism response sex stem cells trend vaping vegetable glycerin

项目摘要

Abstract E-cigarette devices produce an aerosol from e-liquids containing flavorings, nicotine, and vehicle. Inhaled e- cigarette aerosol can reach the alveolar region. Alveolar type II (ATII) cells produce and secrete pulmonary surfactant, which decreases surface tension. They also have a stem cell potential, proliferate and repair the epithelium after damage leading to lung regeneration. Due to their energy-demanding functions and location in the lung, they depend highly on mitochondria. Mitochondrial DNA lacks histones that serve as a barrier against damaging factors, contributing to its susceptibility to damage. Mitochondrial dysfunction can lead to mitophagy and ATII cell death. Our preliminary results in the parent R01 grant and this application demonstrate the harmful effect of e-cigarette aerosols with fruit and dessert flavors on human primary ATII cells. The goal of this administrative supplement proposal is to clarify further the sex influences on human primary ATII cell dysfunction caused by exposure to flavored constituents and e-cigarette aerosols. In Aim 1, we will compare DNA damage in ATII cells exposed to flavored constituents and e-cigarette aerosols with fruit and dessert flavors. In Aim 2, we will define the impact of this exposure on mitochondrial function in ATII cells. Obtained results will define sex influences on the respiratory injury risk of flavored constituents and e-cigarette aerosols.

抽象的电子烟装置从含有香料、尼古丁和媒介物的电子液体中产生气雾。吸入电子香烟气溶胶可以到达肺泡区域。肺泡 II 型 (ATII) 细胞产生并分泌肺泡表面活性剂，可降低表面张力。它们还具有干细胞潜力，能够增殖和修复损伤后的上皮细胞导致肺再生。由于它们的能源需求功能和位置肺部，它们高度依赖线粒体。线粒体 DNA 缺乏作为屏障的组蛋白破坏因素，导致其容易受到损害。线粒体功能障碍可导致线粒体自噬和 ATII 细胞死亡。我们在母公司 R01 拨款和本申请中的初步结果证明了有害的带有水果和甜点口味的电子烟气雾剂对人类原代 ATII 细胞的影响。此举的目标行政补充提案旨在进一步阐明性别对人类原代ATII细胞功能障碍的影响由接触调味成分和电子烟气溶胶引起。在目标 1 中，我们将比较 DNA 损伤在暴露于风味成分以及带有水果和甜点风味的电子烟气雾剂的 ATII 细胞中。在目标 2 中，我们将确定这种暴露对 ATII 细胞线粒体功能的影响。获得的结果将定义性别调味成分和电子烟气溶胶对呼吸道损伤风险的影响。