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蛋白质酶功能与e-cig蒸汽凝聚物挑战的肺上皮细胞中的炎症反应之间的相互作用

R Begum¹, S Thota¹, S Batra²

¹Laboratory of Pulmonary Immunotoxicology, Department of Environmental Toxicology, Southern University and A&M College, 129 Health Research Center, Baton Rouge, Louisiana, 70813, USA.

Archives of toxicology

|June 21, 2023

概括

电子烟蒸汽通过改变蛋白酶子单元,特别是LMP7,从而诱导肺细胞的氧化应激和炎症反应,从而诱导炎症. 抑制LMP7可以减少这些影响,这表明它在电子烟引起的肺损伤中起着关键作用.

科学领域:

肺部毒理学肺部毒理学
细胞免疫学细胞免疫学
分子生物学分子生物学

背景情况:

电子烟 (e-cigs) 越来越受欢迎,其蒸汽可以引起肺炎和氧化应激.
蛋白质酶体是一个降解蛋白质的复合体,具有可诱导的子单元 (免疫蛋白质酶体),对免疫反应至关重要.
像IFN-γ和TNF-α这样的炎症性细胞因子可以提高免疫蛋白酶子单元的调节.

研究的目的:

研究蛋白质酶子单元,特别是LMP7在电子烟蒸汽凝聚物 (ECVC) 诱导的人类膜上皮细胞炎症中的作用 (A549).
探索ECVC暴露,氧化应激和蛋白质酶子单元和炎症媒介体的表达之间的关系.

主要方法:

A549细胞暴露在过空气或含有尼古丁或不含尼古丁的烟草香味ECVC中.
分析了炎症性细胞因子 (IFN-γ,TNF-α) 和蛋白质酶子单元 (构成性和可诱导性) 的水平.
利用LMP7的基因淘汰和LMP7抑制剂 (ONX-0914) 来评估它们对ECVC诱导变化的影响.

主要成果:

ECVC暴露增加了IFN-γ,TNF-α和可诱导蛋白酶子单元 (LMP7,LMP2,MECL1),同时减少了组成子单元.
LMP7敲击逆转了ECVC诱导的NADPH氧化酶和免疫蛋白酶子单元表达.
抑制LMP7降低了NOX亚单元mRNA和炎症性细胞因子/化学因子的释放 (IL-6,IL-8,CCL2,CCL5).

结论:

在ECVC暴露期间,LMP7在调节炎症媒介表达方面发挥着重要作用.
这些发现支持了ECVC挑战细胞中蛋白质酶依赖的,反应性氧物种 (ROS) 介导的炎症模型.
准LMP7可能为电子烟引起的肺炎提供治疗策略.

关键词:

抗氧化剂是一种抗氧化剂.细胞因子 (cytokines) 是一种细胞因子.电子烟是电子烟的产品.蛋白质组是蛋白质组中的一个.这就是ROSOS ROS.

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