Al-Sawalha Nour A, Migdadi Ala'a M, Alzoubi Karem H, Khabour Omar F, Qinna Nidal A
a Faculty of Pharmacy , Jordan University of Science and Technology , Irbid , Jordan.
b Faculty of Applied Medical Sciences , Jordan University of Science and Technology , Irbid , Jordan.
Inhal Toxicol. 2017 Feb;29(2):46-52. doi: 10.1080/08958378.2017.1280105. Epub 2017 Feb 28.
There has been an increase in the popularity of waterpipe tobacco smoking (WTS) worldwide, especially in the younger population, including asthma patients. In this study, we investigated the effects of waterpipe smoking on airway inflammation, cytokine levels and oxidative stress markers in an antigen-driven murine model of asthma.
Balb/c mice were divided into four groups; (1) control (received fresh air, ovalbumin sensitization and saline challenge), (2) WTS (received WTS, ovalbumin sensitization and saline challenge), (3) Ova S/C (received fresh air, ovalbumin sensitization and ovalbumin challenge) and (4) simultaneous WTS and Ova S/C (received WTS, ovalbumin sensitization and ovalbumin challenge). Airway inflammatory cells were evaluated in the broncho-alveolar lavage fluid. Cytokines [interleukin (IL)-13, 10 and 18] and oxidative stress markers [superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx)] were evaluated in the lung homogenates.
Chronic exposure to WTS significantly increased the number of airway inflammatory cells in mice, specifically: eosinophils, neutrophils, macrophages and lymphocytes. The level of IL-13 in the lungs was increased and the level of IL-10 was reduced (p < 0.05) by WTS. Chronic WTS potentiated the increase in inflammatory cells induced by Ova S/C (p < 0.05). The level of IL-13 in the lungs was increased by simultaneous WTS and Ova S/C (p < 0.05) while, levels of IL-10, IL-18, SOD, catalase and GPx in the lungs were not affected.
Chronic WTS exposure induced airway inflammation in control mice and enhanced airway inflammation in murine model of asthma.
水烟吸食（WTS）在全球范围内越来越流行，尤其是在年轻人群体中，包括哮喘患者。在本研究中，我们在抗原驱动的哮喘小鼠模型中研究了水烟吸食对气道炎症、细胞因子水平和氧化应激标志物的影响。
将Balb/c小鼠分为四组；（1）对照组（接受新鲜空气、卵清蛋白致敏和生理盐水激发），（2）水烟吸食组（接受水烟吸食、卵清蛋白致敏和生理盐水激发），（3）卵清蛋白致敏/激发组（接受新鲜空气、卵清蛋白致敏和卵清蛋白激发）和（4）水烟吸食与卵清蛋白致敏/激发同时进行组（接受水烟吸食、卵清蛋白致敏和卵清蛋白激发）。对支气管肺泡灌洗液中的气道炎症细胞进行评估。对肺匀浆中的细胞因子[白细胞介素（IL）-13、10和18]和氧化应激标志物[超氧化物歧化酶（SOD）、过氧化氢酶和谷胱甘肽过氧化物酶（GPx）]进行评估。
长期暴露于水烟吸食显著增加了小鼠气道炎症细胞的数量，具体为：嗜酸性粒细胞、中性粒细胞、巨噬细胞和淋巴细胞。水烟吸食使肺中IL-13水平升高，IL-10水平降低（p < 0.05）。长期水烟吸食增强了卵清蛋白致敏/激发诱导的炎症细胞增加（p < 0.05）。水烟吸食与卵清蛋白致敏/激发同时进行使肺中IL-13水平升高（p < 0.05），而肺中IL-10、IL-18、SOD、过氧化氢酶和GPx水平未受影响。
长期暴露于水烟吸食可诱导对照小鼠气道炎症，并加重哮喘小鼠模型的气道炎症。
